Endogenous opiates and the pathogenesis of hypertension.
Opiates are now known to be important modulators of cardiovascular function in both the normotensive and hypertensive states. There is accumulating evidence that endogenous opiates are elevated in models of hypertension of various etiologies including genetic and renovascular hypertension. Early evidence for elevated opiates in hypertension arose from observations that hypertensive humans and rats with genetic or experimental hypertension exhibited hypoalgesia in various tests of pain sensitivity. Because pain and cardiovascular regulatory systems have in common a number of brain loci, cardiovascular effects of opiates and opiate blockade were studied. These studies have shown that opiate blockade can attenuate the development of hypertension and reduce blood pressure in chronic hypertension possibly via actions on the baroreflexes and/or by modulating the centrally mediated pressor actions of angiotensin II.
Szilagyi
J E
JE
Department of Pharmacology, University of Houston, Texas 77204-5515.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002319:Cardiovascular System / Q000503:physiopathology; D004723:Endorphins / Q000378:metabolism / Q000502:physiology*; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D006978:Hypertension, Renovascular / Q000209:etiology / Q000503:physiopathology; D008955:Models, Cardiovascular; D009270:Naloxone / Q000494:pharmacology; D009294:Narcotics / Q000494:pharmacology; D010146:Pain / Q000503:physiopathology; D011311:Pressoreceptors / Q000502:physiology; D012769:Shock / Q000401:mortality / Q000503:physiopathology
D004723:Endorphins; D009294:Narcotics; D000804:Angiotensin II; D009270:Naloxone