Vascular changes in hypertension in response to drug treatment: Effects of angiotensin receptor blockers.
Large and small arteries are remodelled in hypertension - their structure, function and mechanics are altered. These changes contribute to elevated blood pressure and to the complications of hypertension. The present paper concentrates on small (resistance) artery changes in hypertension. In hypertension, these vessels exhibit a form of remodelling known as 'eutrophic' remodelling, in which smooth muscle cells are restructured around a smaller lumen, without true hypertrophy, particularly in milder forms of hypertension. Changes in these small arteries are the first manifestation of target organ damage in patients with hypertension. In more severe forms of hypertension and in secondary hypertension, hypertrophic remodelling has been reported. Stiffness of the vessel wall may be decreased initially; later, as hypertension becomes more severe, the wall of resistance vessels may become stiffer. Endothelial dysfunction occurs in a percentage of patients, similar to the prevalence of left ventricular hypertrophy. Interruption of the renin-angiotensin system may correct many of these abnormalities. The present report investigated the effects of angiotensin type 1 (AT1) receptor antagonists on small arteries of hypertensive patients compared with the beta-blocker atenolol in different studies. Beta-blocker treatment did not modify either the structure or the function of small arteries in contrast to the AT1 antagonist losartan in a double-blind, randomized, one-year study. Patients previously treated with atenolol to lower blood pressure, but whose small artery structure and function did not improve, were examined. These hypertensive patients were switched to the AT1 antagonist irbesartan for one year. Gluteal subcutaneous biopsies showed that the structure and endothelial function of small arteries that had remained altered by atenolol treatment were corrected by irbesartan treatment, although blood pressure control with irbesartan was identical to that previously achieved with atenolol. Improved outcomes in clinical trials using angiotensin-converting enzyme inhibitors and AT1 receptor antagonists may be a result of the vascular protective effects offered by these agents.
Schiffrin
Ernesto L
EL
Clinical Research Institute of Montreal, Montreal, Canada. schiff@ircm.qc.ca
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001158:Arteries / Q000187:drug effects* / Q000503:physiopathology*; D001262:Atenolol / Q000494:pharmacology / Q000627:therapeutic use; D001713:Biphenyl Compounds / Q000494:pharmacology / Q000627:therapeutic use; D017315:Cilazapril / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D000077405:Irbesartan; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use; D020913:Perindopril / Q000494:pharmacology / Q000627:therapeutic use; D013777:Tetrazoles / Q000494:pharmacology / Q000627:therapeutic use
D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D001713:Biphenyl Compounds; D013777:Tetrazoles; D017315:Cilazapril; D001262:Atenolol; D000077405:Irbesartan; D019808:Losartan; D020913:Perindopril