Epinephrine and norepinephrine contents of tissues and perfusates have been measured by fluorimetric methods to ascertain which catecholamine is the sympathetic transmitter in bullfrogs and turtles. Except for adrenal and sympathetic chain, the predominant catecholamine in bullfrogs is epinephrine. In snapping turtles, norepinephrine predominates. During perfusion of bullfrog heart or liver without stimulation, only traces of catecholamine appear in perfusates, whereas during sympathetic nerve stimulation a large output of epinephrine occurs. In the bullfrog epinephrine rather than norepinephrine seems to be the sympathetic mediator. The situation may be the reverse in the turtle. Environmental temperature did not alter bullfrog tissue catecholamine. Cardiac sympathetic denervation did not decrease myocardial catecholamine within 6 weeks at low temperatures, but in animals maintained at 20 C survival was not achieved. Epinephrine levels in bullfrog ventricle were not lowered by 5 hr of contractions induced by electrical stimulation at 30/min compared with controls in arrest. The fact that myocardial catecholamine stores are not depleted by contractile activity may result either from absence of utilization or from equivalence between breakdown and synthesis.

SUMMARY Prerious studies have suggested that angiotensin II and sodium can act as alternative mechanisms in maintaining high blood pressure in chronic renovascular hypertension. In the present study, exchangeable sodium was measured in rats in which angiotensin II had been confirmed or excluded as the main cause of the hypertension. To determine the degree of participation of angiotensin II in the maintenance of the high blood pressure, we studied the mean blood pressure response to an angiotensin antagonist (l-Sar-8-Alaangiotensin II) and to a converting enzyme inhibitor (SQ20.881). Rats with a decrease hi blood pressure of less than 20 mm Hg, in response to both inhibitors, were classified as nonresponders; those with a decrease of 20 mm Hg or more, as responders. Fifty percent of the rats with two-kidney hypertension were nonrespooders, and they had lower blood pressure and plasma renin activity than the responders. Further, these two-kidney, hypertensive, nonresponder rats had normal exchangeable sodium. The two-kidney hypertensive responders, on the other hand, had significantly higher exchangeable sodium than both the two-kidney, hypertensive nonresponders and the two-kidney control rats. These results suggest that angiotensin II and exchangeable sodium do not play a major role in the maintenance of the high Mood pressure in the two-kidney hypertensive nonresponders. However, there appears to be an abnormal relationship between renin and exchangeable sodium in the two-kidney hypertensive responders that could contribute to the maintenance of the hypertension. differing roles in the pathogenesis of the maintenance of high blood pressure in oneas compared to two-kidney hypertensive rats (one renal artery constricted and the contralateral kidney removed or untouched, respectively). In one-kidney hypertensive rats, sodium retention appears to be the main pathogenetic factor in the chronic phase of the hypertension. In fact, Tobian et al. 1 have reported an increase in exchangeable sodium, and Swales et al. model of hypertension in rats. In the two-kidney model, angiotensin has been considered the most important pathogenetic factor.3 However, in previous work, we have found that in rats with moderate, chronic, two-kidney hypertension, the maintenance of high blood pressure does not always depend on the pressor effect of angiotensin II, since many rats do not respond to the administration of an angiotensin antagonist* or a converting enzyme inhibitor (CEI) with a decrease in blood pressure.8 Furthermore, MShring et al. 8 have reported a positive cumulative sodium balance and a positive correlation between the increase in blood pressure and sodium retention in rats with moderate two-kidney hypertension.It could be that the high blood pressure in the twokidney model is maintained by a dual mechanism: one related to sodium metabolism when the hypertension is moderate, and the other to the renin-angiotensin system when the hypertension is more severe. To further advance this hypothesis, in the present study we measu...

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SUMMARY The purpose of this study was twofold: 1) to determine whether the failure of rats with chronic renovascular hypertension to respond to the angiotensin II antagonist (AHA) with a decrease in mean blood pressure (BP) was due to the agonistic effect of the antagonist; and, 2) if this was not the case, to examine whether a positive sodium balance impaired the reversal of the hypertension, after unclamping, in the rats that did not respond to angiotensin inhibitors. For this purpose, rats with chronic, two-kidney Goldblatt hypertension (one renal artery clamped and contraJateral untouched) were tested for their BP response to the AHA (1-Sar-8-Ala-angiotensin II) and to the converting enzyme inhibitor (CEI) SQ20,881, which is devoid of agonistic effect. Approximately 50% of the rats responded to both inhibitors either with no change or with a decrease in BP of less than 20 mm Hg (nonresponders). The other 50% had a decrease in BP of 20 mm Hg or greater (responders). The decrease in BP produced by the AHA and the CEI correlated significantly (r = 0.76). Nonresponders to both inhibitors were undamped or sham undamped. A positive sodium balance was produced before surgery by injecting either 400 or 1000 /iEq of sodium and was maintained for 12 hours. Direct BP significantly decreased 12 hours after surgery in the undamped rats despite a continuous positive sodium balance. In the sham undamped rats, BP did not change. These data indicate that the failure to respond to the AHA is not due to the agonistic effect of this peptide. Furthermore, these data suggest that a positive sodium balance is not a major patbogenetic factor in maintaining the high BP in the nonresponder rats, since a positive sodium balance failed to maintain the hypertension after unclamping. while leaving the contralateral kidney untouched, produced hypertension (two-kidney renal hypertension) in rats.1 Evidence 25 suggests that the renin-angiotensin system participates in the pathogenesis of the development of this type of hypertension. However, the factors that contribute to the maintenance of high blood pressure in the chronic phase of the hypertension are not well determined. The role of the renin-angiotensin system in the pathogenesis of this phase of renovascular hypertension has been extensively studied by inhibiting this system with antibodies against renin"' 7 or angiotensin JJJ, s-ii or w j t }, angiotensin antagonists 2 ' *• 1216 and converting enzyme inhibitor (CEI). 389 that some rats 15 or even patients 1719 with chronic moderate hypertension, do not respond to the inhibition of the renin-angiotensin system, but do respond to renal revascularization with a decrease in blood pressure.The role of sodium and water retention has also been studied in the two-kidney model. Tobian et al. 20 found that exchangeable sodium was normal. Swales et al. 21 ' n noted a negative or normal cumulative sodium balance and also found that removal of sodium by peritoneal dialysis had no effect on the blood pressure. However, in these sodium metabol...