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Renovascular Hypertension Medication

  • Author: Rebecca J Schmidt, DO, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: May 13, 2016
 

Medication Summary

Medical treatment of renovascular hypertension (RVHT) may be necessary to control blood pressure until surgery can be performed. Attempts should be made to reduce the blood pressure before surgery so as to improve the likelihood of a good surgical outcome. Afterward, medical treatment is necessary 25-30% of the time to provide complete resolution of improved or refractory hypertension.

Adrenergic receptor blockers and diuretics are the preferred agents. Arterial dilators are also useful in the preoperative management of malignant hypertension. Calcium channel blockers do not seem to be as widely used, and angiotensin-converting enzyme (ACE) inhibitors are generally avoided because of their potential to compromise renal function.

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ACE Inhibitors

Class Summary

ACE inhibitors have been used by some in the control of RVHT. These agents minimize an ischemia-induced rise in angiotensin production. Because hypertension may be dependent on angiotensin II, antihypertensives that inhibit renin or angiotensin II are used widely. All drugs in this class have similar action and adverse effects. In particular, ACE inhibitors increase the risk of decreased renal function. Although this increased risk is usually reversible, the use of these agents is generally avoided until definitive therapy has been attempted.

Renal blood flow is maintained by a balance between angiotensin-II–induced vasoconstriction and prostaglandin-mediated vasodilation. With ACE inhibitors, kidney perfusion is increased and renal vascular resistance decreased. ACE inhibitors induce vasodilation in both afferent and efferent arterioles. The glomerular filtration rate (GFR) generally increases. However, in hypoperfusion states (eg, renal artery stenosis (RAS), aggressive diuresis, and decompensated congestive heart failure), GFR may fall because of unopposed prostaglandin vasodilation.

Captopril

 

Captopril, the most commonly used ACE inhibitor, prevents conversion of angiotensin I to angiotensin II (a potent vasoconstrictor), resulting in lower aldosterone secretion. It is excreted primarily by the kidney.

Enalapril (Vasotec)

 

Enalapril is a competitive ACE inhibitor that reduces angiotensin II levels and decreases aldosterone secretion.

Lisinopril (Zestril, Prinivil)

 

Lisinopril prevents conversion of angiotensin I to angiotensin II, resulting in decreased aldosterone secretion.

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Angiotensin Receptor Blockers (ARBs)

Class Summary

Angiotensin II is the primary vasoactive hormone of the renin-angiotensin-aldosterone system (RAAS) and plays an important role in the pathophysiology of hypertension. Besides being a potent vasoconstrictor, angiotensin II stimulates aldosterone secretion by the adrenal gland; thus, angiotensin receptor blockers (ARBs) decrease systemic vascular resistance without a marked change in heart rate by blocking the effects of angiotensin II.

Type I angiotensin receptors are found in many tissues, including vascular smooth muscle and the adrenal gland. Type II angiotensin receptors also are found in many tissues, although their relationship to cardiovascular hemostasis is not known. The affinity of ARBs for the type I angiotensin receptor is approximately 1000 times greater than that for the type II angiotensin receptor.

In general, ARBs do not inhibit ACE, other hormone receptors, or ion channels. They interfere with the binding of formed angiotensin II to its endogenous receptor. Experience with using ARBs to treat RVHT is still limited. Losartan and valsartan are specific and selective nonpeptide ARBs that block the vasoconstricting and aldosterone-secreting effects of angiotensin II.

Other ARBs have been approved by the US Food and Drug Administration (FDA), including olmesartan (Benicar). Olmesartan is initiated at a dosage of 20 mg/day orally, which may be increased to 40 mg/day after 2 weeks if further blood pressure reduction is required.

Losartan (Cozaar)

 

Losartan is appropriate for patients unable to tolerate ACE inhibitors. It may induce a more complete inhibition of the RAAS than ACE inhibitors do, it does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema. Compared to the ACE inhibitors (eg, captopril and enalapril), losartan is associated with a lower incidence of drug-induced cough, rash, and taste disturbances.

Valsartan (Diovan)

 

Valsartan is appropriate for patients unable to tolerate ACE inhibitors. It may induce a more complete inhibition of the RAAS than ACE inhibitors do, it does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema. Compared to the ACE inhibitors (eg, captopril and enalapril), losartan is associated with a lower incidence of drug-induced cough, rash, and taste disturbances.

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Blockers, Beta-1 Selective

Class Summary

Adrenergic blockers (both alpha-adrenergic and beta-adrenergic) compete with adrenergic neurotransmitters (eg, catecholamines) for binding at sympathetic receptor sites. They tend to be some of the most effective medicines for prolonged treatment of RVHT.

At low doses, alpha-adrenergic receptor blockers may be used as monotherapy in the treatment of hypertension. At higher doses, they may cause sodium and fluid to accumulate. As a result, concurrent diuretic therapy may be required to maintain the hypotensive effects of the alpha-receptor blockers.

Atenolol and metoprolol, in low doses, selectively block beta1 -adrenergic receptors in the heart and vascular smooth muscle. Pharmacodynamic consequences of beta1 -receptor blockade include decreases in (1) resting and exercise heart rate, (2) cardiac output, and (3) systolic and diastolic blood pressure. Like all selective adrenergic antagonists, they lose their selectivity for the beta1 receptor higher doses and can competitively block beta2 -adrenergic receptors in the bronchial and vascular smooth muscles, potentially causing bronchospasm.

Actions that generally make beta blockers useful in treating hypertension include a negative chronotropic effect that decreases the heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, reduction of sympathetic outflow from the central nervous system (CNS), and suppression of renin release from the kidneys. Thus, beta blockers affect blood pressure via multiple mechanisms.

Metoprolol (Lopressor, Toprol-XL)

 

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.

Atenolol (Tenormin)

 

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 types.

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Beta-Blockers, Nonselective

Class Summary

Although selective beta1 -blockers (eg, metoprolol) are preferred over nonselective agents in patients with asthma or pulmonary conditions in which acute bronchospasm would put them at risk (eg, chronic obstructive pulmonary disease [COPD], emphysema, or bronchitis), all beta-blockers should be used with caution in these patients, particularly with high-dose therapy.

Propranolol (Inderal, InnoPran XL)

 

Propranolol is a beta-adrenergic blocking agent. Renin release is enhanced by beta-receptor activation, and chronic beta blockade consistently suppresses plasma renin activity. Propranolol has membrane-stabilizing activity and decreases the automaticity of contractions. It is not suitable for emergency treatment of hypertension and should not be administered IV in hypertensive emergencies.

Labetalol (Trandate)

 

Labetalol blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic receptor sites.

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Alpha Blockers, Antihypertensives

Class Summary

At low doses, alpha-adrenergic receptor blockers may be used as monotherapy in the treatment of hypertension. At higher doses, they may cause sodium and fluid to accumulate. As a result, concurrent diuretic therapy may be required to maintain the hypotensive effects of alpha-receptor blockers.

Phentolamine

 

Phentolamine is an alpha1- and alpha2-adrenergic blocking agent that antagonizes the action of circulating epinephrine and norepinephrine, reducing the hypertension that results from catecholamine's effects on the alpha-receptors.

Phenoxybenzamine (Dibenzyline)

 

Phenoxybenzamine is a noncompetitive alpha-adrenergic blocker. It is a long-acting adrenergic alpha-receptor blocker that can produce and maintain a chemical sympathectomy. Phenoxybenzamine hydrochloride lowers supine and upright blood pressure. It does not affect the parasympathetic nervous system.

Prazosin (Minipress)

 

Prazosin is an alpha blocker. It decreases arterial tone by allowing peripheral postsynaptic blockade.

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Calcium Channel Blockers

Class Summary

Calcium channel blockers provide control of hypertension associated with less impairment of function of the ischemic kidney. It has been suggested that they may have beneficial long-term effects, but this remains uncertain.

Calcium channel blockers inhibit influx of extracellular calcium across both myocardial and vascular smooth muscle cell membranes. Serum calcium levels remain unchanged. The resultant decrease in intracellular calcium inhibits the contractile processes of myocardial smooth muscle cells, resulting in dilation of coronary and systemic arteries and improved oxygen delivery to myocardial tissue. In addition, total peripheral resistance, systemic blood pressure, and afterload are decreased.

Diltiazem (Cardizem CD, Dilacor XR, Tiazac)

 

Diltiazem is similar to verapamil in that it inhibits the influx of extracellular calcium across both the myocardial and vascular smooth muscle cell membranes.

Verapamil (Calan, Verelan, Covera-HS)

 

During depolarization, verapamil inhibits calcium ions from entering slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium.

Nifedipine (Adalat, Procardia, Procardia XL)

 

Nifedipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Sublingual administration is generally safe, despite theoretical concerns.

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Diuretics, Other

Class Summary

Diuretics promote excretion of water and electrolytes by the kidneys. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention has resulted in edema or ascites. They may be used as monotherapy or combination therapy to treat hypertension. Thiazide diuretics are preferred.

Diuretics are used only as an adjunct to other medications for RVHT, especially during acute hypertensive crises. Furosemide is especially effective in managing pulmonary edema associated with hypertensive crises and may be particularly useful in patients unresponsive to other diuretics or those who have severe renal impairment.

Furosemide (Lasix)

 

Furosemide primarily appears to inhibit reabsorption of sodium and chloride in the ascending limb of the loop of Henle. These effects increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs after administration of furosemide. Renal vascular resistance decreases, and renal blood flow is enhanced.

Hydrochlorothiazide (Microzide)

 

Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water and potassium and hydrogen ions.

Bumetanide

 

Bumetanide increases excretion of water by interfering with the chloride-binding cotransport system; this, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle. Bumetanide does not appear to act in the distal renal tubule.

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Vasodilators

Class Summary

Arterial vasodilators are effective in reducing hypertension and may be useful in the short-term management of RVHT before surgical treatment. Nitroprusside is especially useful for this purpose.

Nitroprusside (Nitropress)

 

Nitroprusside produces vasodilation and increases the inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing the heart rate. It is mainly used when a patient presents with a hypertensive emergency secondary to RVHT.

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Cardiovascular, Other

Class Summary

Renin inhibitors constitute the newest class of antihypertensive drugs. They act by disrupting the RAAS feedback loop.

Aliskiren (Tekturna)

 

Aliskiren is a direct renin inhibitor. It decreases plasma renin activity and inhibits the conversion of angiotensinogen to angiotensin I (thus also decreasing angiotensin II) and thereby disrupts the RAAS feedback loop. Aliskiren is indicated for treatment of hypertension, either alone or in combination with other antihypertensive drugs.

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Contributor Information and Disclosures
Author

Rebecca J Schmidt, DO, FACP, FASN Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, West Virginia State Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Muhammad R Mustafa, MD Assistant Professor of Medicine, Section of Nephrology, West Virginia University Health Sciences Center

Muhammad R Mustafa, MD is a member of the following medical societies: American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation

Disclosure: Nothing to disclose.

Andre Hebra, MD Chief, Division of Pediatric Surgery, Professor of Surgery and Pediatrics, Medical University of South Carolina College of Medicine

Andre Hebra, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Association for Academic Surgery, Society of Laparoendoscopic Surgeons, South Carolina Medical Association, Southeastern Surgical Congress, and Southern Medical Association

Disclosure: Nothing to disclose.

Mary C Mancini, MD, PhD Professor and Chief, Cardiothoracic Surgery, Department of Surgery, Louisiana State University Health Sciences Center-Shreveport

Mary C Mancini, MD, PhD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons, and Southern Surgical Association

Disclosure: Nothing to disclose.

John Myers, MD Director, Pediatric and Congenital Cardiovascular Surgery, Departments of Surgery and Pediatrics, Professor, Penn State Children's Hospital, Milton S Hershey Medical Center

John Myers, MD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Cardiology, American College of Surgeons, American Heart Association, American Medical Association, Congenital Heart Surgeons Society, Pennsylvania Medical Society, and Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Jonah Odim, MD, PhD, MBA Senior Medical Officer, Transplantation Immunology Branch, Division of Allergy, Immunology, and Transplantation, National Institute of Allergy and Infectious Diseases, National Institutes of Health

Jonah Odim, MD, PhD, MBA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physician Executives, American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, Association for Academic Surgery, Association for Surgical Education, Canadian Cardiovascular Society,International Society for Heart and Lung Transplantation, National Medical Association, New York Academy of Sciences, Royal College of Physicians and Surgeons of Canada, Society of Critical Care Medicine, and Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

L Michael Prisant, MD, FACC Director of Hypertension and Clinical Pharmacology Unit, Professor of Medicine, Department of Medicine, Medical College of Georgia

L Michael Prisant, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Clinical Pharmacology, American College of Forensic Examiners, American College of Physicians, American Heart Association, and American Medical Association

Disclosure: Abbott Grant/research funds Investigator; Boehringer-Ingelheim Grant/research funds Other; Eli Lilly None Investigator; Novartis None Investigator; Abbott, Boehringer-Ingelheim, Forest, Gilead, Merck, Merck/Schering-Plough, Novartis, Oscient, Sciele, SunTech Medical Consulting fee Consulting; Abbott, Boehringer-Ingelheim, Merck, Merck/Schering-Plough, Novartis, Oscient Honoraria Speaking and teaching

Sandeep S Soman, MBBS, MD, DNB Senior Staff Physician, Department of Internal Medicine, Division of Nephrology and Hypertension, Henry Ford Hospital

Sandeep S Soman, MBBS, MD, DNB is a member of the following medical societies: American College of Physicians, American Medical Association, and American Society of Nephrology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Patrick B Thomas, MD Fellow, Department of Pediatric Surgery, Texas Children's Hospital

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Magnetic resonance angiography (MRA) showing renal artery stenosis. Courtesy of Patricia Stoltzfus, MD, Chief of Interventional Radiology, West Virginia University.
Proposed pathogenesis of renovascular hypertension.
Angiogram showing bilateral renal artery stenosis. Courtesy of Department of Radiology, Henry Ford Hospital.
After percutaneous transluminal angioplasty (right renal artery). Courtesy of Department of Radiology, Henry Ford Hospital.
After percutaneous transluminal angioplasty and stent placement (left renal artery). Courtesy of Department of Radiology, Henry Ford Hospital.
Close-up of the Palmaz stent. Courtesy of Department of Radiology, Henry Ford Hospital.
Aortogram of 4-year-old child with renovascular hypertension caused by stenosis of left renal artery. Note that left kidney has 2 renal arteries and that artery to superior pole has stenosis.
Close-up view of aortogram of 4-year-old child. Stenotic lesion begins at ostium of left superior renal artery. This lesion was caused by fibromuscular dysplasia and did not respond well to balloon angioplasty.
Operative photograph of 4-year-old child. Patient underwent aortorenal bypass with reinforced saphenous vein graft. Inferior pole renal artery was preserved.
Aortogram of 8-year-old child with neurofibromatosis and renovascular hypertension caused by right renal artery stenosis.
Operative photograph of 8-year-old child. Aortorenal bypass was performed with Dacron-reinforced saphenous vein graft. Aorta is completely exposed, and graft is visible inferior to native renal artery.
Although nephrectomy is rarely indicated in treatment of renovascular hypertension in children, it can be safely performed with modern pediatric surgical laparoscopy technique. This 3-month-old child with renal dysplasia and refractory hypertension underwent laparoscopic nephrectomy. Photograph illustrates patient positioning and placement of small trocars at time of nephrectomy. Dysplastic kidney was easily removed through slightly enlarged umbilical incision.
3-month-old child immediately after laparoscopic nephrectomy. This patient was discharged from hospital 2 days after surgery. This approach eliminates need for large incisions and facilitates recovery from surgery, minimizing pain and length of hospital stay.
 
 
 
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