Abstract
The renin angiotensin system and the sympathetic nervous system (SNS) are
essential for sodium homeostasis in man, and their independent roles in this respect are well established. However, recent animal evidence suggests that angiotensin II (Ang II) may interact with the SNS via several mechanisms that could play a role in mediating changes in sodium excretion. We have therefore sought evidence of such an interaction in man by examining the effect of prazosin (PRZ), an a, adrenergic antagonist, on the anti-natriuretic effect of Ang II. We used prazosin and Ang II,both in low doses (0-25 mg and 1 ng/kg per min respectively) so that systemic blood pressure was not altered by either.
Eight salt-replete male volunteers (mean age + S.E.M. 23 + 2 yr; 24 h urinary Na+ excretion: 176 + 20 mmol/24 h) were studied on 4 occasions at least 7 days apart. Subjects were given an initial water load of 20 ml kg-' body weight and thereafter ingested the same volume of water as was passed in the urine. The following treatment combinations were administered in single-blind randomized fashion: glucose 5% used as a placebo (P), PRZ 0-25 mg+ 5 % glucose (P), PRZ + Ang II 1 ng/kg per min, P + Ang II, P + P. Blood pressure (BP) and heart rate (HR) were monitored at regular intervals.
The absolute sodium excretion (UvNa+) [mean + S.E.M.; ,umol/min] at 40 min after the Ang II or P infusion for all four study days were: P + P, 148+15; PRZ + P,169 + 16; Ang JJ+ P, 91 + 7 (P < 0 01 vs placebo using Manova); PRZ + Ang II, 133+21. Systemic BP and HR did not differ between study days.
In conclusion, we have shown that prazosin blunts the anti-natriuretic effect of
Ang II. This suggests that renal a, adrenoreceptors may exert a permissive role on the renal effects of circulating angiotensin II in man.
essential for sodium homeostasis in man, and their independent roles in this respect are well established. However, recent animal evidence suggests that angiotensin II (Ang II) may interact with the SNS via several mechanisms that could play a role in mediating changes in sodium excretion. We have therefore sought evidence of such an interaction in man by examining the effect of prazosin (PRZ), an a, adrenergic antagonist, on the anti-natriuretic effect of Ang II. We used prazosin and Ang II,both in low doses (0-25 mg and 1 ng/kg per min respectively) so that systemic blood pressure was not altered by either.
Eight salt-replete male volunteers (mean age + S.E.M. 23 + 2 yr; 24 h urinary Na+ excretion: 176 + 20 mmol/24 h) were studied on 4 occasions at least 7 days apart. Subjects were given an initial water load of 20 ml kg-' body weight and thereafter ingested the same volume of water as was passed in the urine. The following treatment combinations were administered in single-blind randomized fashion: glucose 5% used as a placebo (P), PRZ 0-25 mg+ 5 % glucose (P), PRZ + Ang II 1 ng/kg per min, P + Ang II, P + P. Blood pressure (BP) and heart rate (HR) were monitored at regular intervals.
The absolute sodium excretion (UvNa+) [mean + S.E.M.; ,umol/min] at 40 min after the Ang II or P infusion for all four study days were: P + P, 148+15; PRZ + P,169 + 16; Ang JJ+ P, 91 + 7 (P < 0 01 vs placebo using Manova); PRZ + Ang II, 133+21. Systemic BP and HR did not differ between study days.
In conclusion, we have shown that prazosin blunts the anti-natriuretic effect of
Ang II. This suggests that renal a, adrenoreceptors may exert a permissive role on the renal effects of circulating angiotensin II in man.
| Original language | English |
|---|---|
| Pages (from-to) | 139P |
| Number of pages | 1 |
| Journal | Journal of Physiology |
| Volume | 430 |
| Publication status | Published - 1990 |
| Event | Physiological Society. Oxford Meeting - Oxford, United Kingdom Duration: 27 Jul 1990 → 28 Jul 1990 |