Peripheral alpha-1 and alpha-2 adrenergic receptors in three models of hypertension in rats: an in vitro autoradiography study.
In vitro autoradiography was used to compare peripheral alpha-1 and alpha-2 adrenergic receptor binding in various tissues using [3H]prazosin and [3H]rauwolscine, respectively, in three models of experimental hypertension in rats. Models studied included two-kidney, one-clip hypertension, one-kidney, one-clip hypertension, desoxycorticosterone-salt hypertension, and three normotensive control groups: two-kidney control, one-kidney control and salt-loaded control. Blood pressures at death were significantly higher in all three hypertensive groups compared with normotensive controls, but there were no significant differences among the hypertensive or normotensive groups. Plasma norepinephrine levels were significantly elevated in all three hypertensive groups compared with respective controls, with no significant differences among hypertensive or control groups. In all three hypertensive groups, there were significant reductions in binding of aortic and mesenteric vascular alpha-1 receptors, renal tubular alpha-1 and alpha-2 receptors, and adrenal cortical alpha-2 receptors when compared with respective control groups. Reduced binding of cardiac ventricular alpha-1 and alpha-2 receptors was also found in all hypertensive groups, but not to statistically significant levels. No significant differences in intestinal alpha-1 and alpha-2 receptor binding were detected in either hypertensive or normotensive groups. The results suggest increased peripheral sympathetic activity in all three models of experimental hypertension, which is associated with down-regulation of alpha-1 and alpha-2 receptors in a number of peripheral tissues, especially those that control cardiovascular hemodynamics and fluid and salt balance. There is no evidence of an increase in peripheral alpha receptor binding as has often been found in some models of genetic or spontaneous hypertension.
Wilson
S K
SK
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
D000311:Adrenal Glands / Q000737:chemistry; D000818:Animals; D001345:Autoradiography; D001794:Blood Pressure; D001808:Blood Vessels / Q000737:chemistry; D003900:Desoxycorticosterone / Q000494:pharmacology; D006973:Hypertension / Q000209:etiology / Q000378:metabolism*; D007668:Kidney / Q000737:chemistry; D008297:Male; D009206:Myocardium / Q000737:chemistry; D009638:Norepinephrine / Q000097:blood; D011224:Prazosin / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000032:analysis*; D015016:Yohimbine / Q000378:metabolism
D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D003900:Desoxycorticosterone; D009638:Norepinephrine; D011224:Prazosin