To avoid complicating systemic effects, the influence of adrenergic hormones on renin secretion was examined in the isolated rat kidney perfused with Krebs-dextran solution at a constant mean pressure and flow rate. Isoproterenol and glucagon produced a consistent increase in renin secretion without a change in perfusion pressure and flow. Similarly the increase in renin secretion with norepinephrine, which was associated with intense vasoconstriction and raised perfusion pressure, was still observed after the vasoconstrictive effect was abolished with phenoxybenzamine. Isoproterenol- stimulated renin secretion, unaffected by phenoxybenzamine, was markedly suppressed by dl -propranolol but not by d -propranolol. The failure of dl -propranolol to suppress the renin response to glucagon confirms observations in other tissues and suggests involvement of other receptors or alternative mechanisms. These findings support a direct intrarenal effect of adrenergic hormones on renin secretion, and this effect may be mediated specifically by beta receptors in the case of catecholamines.

Two interconvertible renins were isolated from extracts of the pig renal cortex at neutral pH and shown to be protein-bound (renin B, molecular weight 60,000) and free (renin A, molecular weight 40,000) forms of renin. The protein-bound form (renin B) gave a much more prolonged pressor response than did the free form (renin A) on direct bioassay in the rat; it could be converted to renin A by the action of various salts or by acidification below pH 3. The renin-binding protein associated with renin B was isolated by DEAE-cellulose column chromatography under special conditions of elution and appeared to be specific for renin. When pig kidneys were perfused in situ with Krebs-Ringer's solution, isoproterenol stimulation (1-8 tig/m\n) resulted in release of renin in the protein-bound form. It is suggested that renin-binding protein may act as a carrier for the transport of renin to local tissue sites of uptake under some circumstances and thus alter the mode of expression of the renin-angiotensin system in vivo to one of local angiotensin generation and effect. KEYWORDS renin-binding protein angiotensin antibodies renin release angiotensin I immunoassay renin bioassay isoproterenol 1 Kindly supplied by Dr. E. Haas, Beaumont Research Laboratories, Mt. Sinai Hospital, Cleveland, Ohio. 4 2 6

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Twenty-four conscious male Wistar rats with hypertension induced by left renal artery clipping (two-kidney hypertension) were infused intravenously with 1-Sar-8-Ala-angiotensin II a competitive angiotensin II antagonist. The spectrum of responses was wide, ranging from a mild elevation in blood pressure to a marked fall in blood pressure, despite effective and specific angiotensin blockade in all cases. The change in blood pressure during 1-Sar-8-Ala-AII infusion activity showed a significant correlation with the level of plasma renin prevailing immediately before the infusion (r = - 0.78, P less than 0.01) but not with the prevailing blood urea level (r = 0.27, 0.1 greater than P greater than 0.05), the drgree of hypertension (r = 0.42, 0.1 greater than P greater than 0.05), or the time since clipping (r = 0.02, P greater than 0.05). There was no significant correlation between the degree of hypertension and the plasma renin activity (r = 0.42, 0.1 greater than P greater than 0.05). In rats with blood pressure drops greater than 20 mm Hg in response to 1-Sar-8-Ala-AII, the final blood pressure level was still above the normotensive range. Excision of the clipped kidney reduced blood pressure to normal or to near normal within 24 hours in all of the rats tested. It is concluded that the degree of dependence of renal hypertension on the renin-angiotensin system is directly related to the increase in circulating angiotensin itself and not to an increase in sensitivity to angiotensin. Other factors appear to be involved in renal clip hypertension in addition to circulating renin and angiotensin, especially when the measured activity of plasma renin is normal.

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S U M M A R Y1. The relationship between circulating plasma angiotensin I1 and plasma aldosterone in man during sodium deficiency has been investigated in normal male subjects by comparing the amounts of the two hormones: (a) after 5 days of sodium restriction with an injection of frusemide on the third day, (b) during intravenous infusions of angiotensin I1 given in normal sodium balance.2. The results show that aldosterone and angiotensin I1 plasma concentrations were both increased by sodium deficiency, but the increase in aldosterone was much greater than was found when angiotensin I1 was infused during normal sodium balance so as to equal or even exceed the plasma angiotensin I1 concentrations of sodium deficiency.3. Other factors capable of increasing aldosterone secretion (plasma Na+, K+ and ACTH) seemed unlikely to account for the discrepancy, nor was there evidence of sufficient increase in adrenal sensitivity during Na+ deficiency.4. It is suggested that some other unknown factor or factors are necessary to account for the full aldosterone response to this stimulus in man.Key words : angiotensin 11, aldosterone, sodium deficiency, plasma aldosterone, plasma angiotensin 11. Gross (1958) postulated that the renin-angiotensin system may mediate the secretion of aldosterone, and shortly thereafter both Laragh and Genest and their co-workers demonstrated independently the specific aldosterone-stimulating effect of infused angiotensin I1 in man

RHC via the AVA is a feasible and safe alternative to PVA. Our experience and rapid adoption support the use AVA as the access site of choice for RHC in uncomplicated patients.