The characteristics and control of the increase in plasma renin activity (PRA) during environmental heating (EH) were determined in 12 unanesthetized, chronically catheterized baboons. Each EH experiment consisted of a 1.5- to 4-h exposure to an ambient temperature of 39-44°C until core temperature (T(c)) reached 39.5-40.0°C. These EH experiments were done on the baboon in an unblocked state and during β-adrenergic receptor blockade produced by propranolol when on normal-to-high salt intake (NHSI) and on low-salt intake (LSI). PRA rose linearly with T(c) during EH, but the increase in PRA was considerably larger when the baboon was on LSI. The PRA-T(c) linear regression coefficients were 2.32 and 5.98 ng angiotension I·ml-1·h-1·°C-1 in NHSI and LSI states, respectively. This rise in PRA during EH was completely eliminated during β-blockade in both NHSI and LSI states. It is concluded that 1) heart stress activates the sympathetic nervous system to stimulate β-receptor-mediated renin secretion by the kidney, 2) this activation is controlled primarily by internal thermoreceptors, and 3) variations in salt intake alters only the magnitude of the increase in PRA during heat stress, not the mechanisms that produce it.
ASJC Scopus subject areas
- Physiology (medical)