Role of alpha 1- and alpha 2-adrenergic receptors in the human hypertensive kidney.
Since it is not known for certain which alpha-adrenergic receptors mediate renal vasoconstriction in human essential hypertension, we infused either doxazosin (n = 7) or yohimbine (n = 7) into the renal arteries of hypertensive subjects immediately prior to diagnostic angiography. Both agents caused an increment in renal blood flow as assessed with the xenon-washout technique. Doxazosin increased renal flow from 342 +/- 36 to 360 +/- 55 ml/min per 100 g (0.05 less than p less than 0.10). Yohimbine enhanced flow from 380 +/- 41 to 485 +/- 63 ml/min per 100 g (p less than 0.01). The effect of yohimbine was significantly greater than that of doxazosin. In a control group (n = 7) receiving only saline, no changes in renal blood flow occurred. Doxazosin enhanced renin secretion in the kidney by 10 +/- 4% over levels in controls (0.05 less than p less than 0.10), whereas yohimbine increased renin release by 80 +/- 23% (p less than 0.01). The latter increase was apparently not due to alterations in flow alone, since the arteriovenous gradient for renin also widened. We conclude that in resting conditions, neurogenic vascular tone in the kidney depends mainly upon activation of alpha 2-adrenergic receptors. Moreover, these receptors exert a tonic inhibitory influence on renin release.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000328:Adult; D017292:Doxazosin; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D008875:Middle Aged; D011224:Prazosin / Q000031:analogs & derivatives / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D012079:Renal Circulation / Q000187:drug effects; D012083:Renin / Q000378:metabolism; D015016:Yohimbine / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D012083:Renin; D017292:Doxazosin; D011224:Prazosin