Control of plasma renin activity in heat-stressed baboons on varied salt intake

Abstract

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 degrees C until core temperature (Tc) reached 39.5-40.0 degrees C. These EH experiments were done on the baboon in an unblocked state and during beta-adrenergic receptor blockade produced by propranolol when on normal-to-high salt intake (NHSI) and on low-salt intake (LSI). PRA rose linearly with Tc during EH, but the increase in PRA was considerably larger when the baboon was on LSI. The PRA-Tc linear regression coefficients were 2.32 and 5.98 ng angiotensin I X ml-1 X h-1 X degrees C-1 in NHSI and LSI states, respectively. This rise in PRA during EH was completely eliminated during beta-blockade in both NHSI and LSI states. It is concluded that heat stress activates the sympathetic nervous system to stimulate beta-receptor-mediated renin secretion by the kidney, this activation is controlled primarily by internal thermoreceptors, and variations in salt intake alters only the magnitude of the increase in PRA during heat stress, not the mechanisms that produce it.

The Renin-Angiotensin System in Patients with Repeated Anaphylactic Reactions during Hymenoptera Venom Hyposensitization and Sting Challenge

“…The Renin-Angiotensin System and Anaphylaxis role o f the RAS as a factor in stabilizing and maintaining cardiovascular functions during shock [12,13,20]. Any ana phylactic reaction clearly means stress to the patient.…”

“…A potential candidate among these regulato ry factors could be the renin-angiotensin system (RAS) which controls blood pressure, fluid and electrolyte bal ance. It has been shown that the RAS, including angioten sin II (ANG II), is involved in different kinds of stress [12] and hemorrhage [13]. Recently, we have shown that the components o f the RAS, renin, angiotensinogen, angioten sin I (ANG I) and ANG II were significantly reduced in pa tients with hymenoptera venom anaphylaxis.…”

Changes in Angiotensin Peptides in Plasma and Urine in Patients with Anaphylaxis

“…All other in vitro or in vivo tests such as radioallergosorbcnt, histamine re lease, or skin tests do not correlate with the itensitv of A R [1,3,9], One may tentatively speculate that patients with hymenoptera venom allergy show an IgE-mediated sensitiza tion as well as some kind of dysregulation in the reninangiotensin-system. This system seems to be downregulated and may be unable to provide enough A N G II to counteract the cardiovascular symptoms of anaphylaxis [5][6][7],…”

Increased Urinary Excretion of Angiotensin during Anaphylactoid Reactions

“…However, the high levels of angiotensin under conditions of anaphylaxis, as observed in our study, might originate from the stimulation of the plasma RAS. According to the data that the RAS is stimulated during stress and hemorrhage we expected an increase in angiotensin in urine after oral prov ocation [12,13].…”

“…It is generated from an giotensin I (ANG I) by angiotensin-converting enzyme. Under physiological conditions, the RAS has many func tions, mostly related to the regulation of blood pressure, fluid and electrolyte homeostasis [10,11], An involvement o f the RAS with increased renin and ANG II plasma levels has been shown in different kinds of stress and hemorrhage [12,13], AR are stress-related situations. Therefore, know ing the importance of the RAS on cardiovascular function we were intrigued to study the role of the RAS during an AR as a counteracting stabilizing factor.…”