Vm. Zayas et al., ADRENERGIC REGULATION OF RENIN SECRETION AND RENAL HEMODYNAMICS DURING DELIBERATE HYPOTENSION IN HUMANS, The American journal of physiology, 265(5), 1993, pp. 60000686-60000692
To assess the relative contributions of neural and nonneural stimuli o
f renin secretion, the effects of an alpha1-agonist, phenylephrine (Ph
e), or a beta-agonist, epinephrine (Epi), on plasma renin activity (PR
A), renal blood flow (RBF), and glomerular filtration rate (GFR) were
compared during sympathetic blockade with epidural hypotensive anesthe
sia [mean arterial blood pressure (MAP) = 60 and 50 mmHg]. Controls (N
aCl) received saline alone to maintain MAP at 50 mmHg. Epi increased P
RA (ng . ml-2 . h-1) from 0.9 +/- 0.6 to 3.0 +/- 1.5 at 60 mmHg MAP an
d 4.7 +/- 1.8 at 50 mmHg MAP, with associated decreases in RBF (-33 an
d -60%, respectively) and GFR (-27 and -53%, respectively). During hyp
otension with Phe and NaCl, PRA and RBF were unchanged from baseline b
ut GFR decreased. Urinary Na excretion decreased comparably in all thr
ee groups. In conclusion, during sympathetic blockade with epidural an
esthesia, marked reductions in both renal perfusion pressure and dista
l nephron Na delivery were insufficient to increase renin secretion. B
eta-Adrenergic stimulation (e.g., Epi) was required to increase PRA. E
pi decreased RBF suggesting an angiotensin II-mediated effect.