Why the study?
Does centrally administered hydrocortisone increase blood pressure, heart rate, and sympathetic nerve firing in rats?
Does centrally administered hydrocortisone increase blood pressure, heart rate, and sympathetic nerve firing in rats?
Centrally administered hydrocortisone stimulates the brain renin-angiotensin system to increase sympathetic nerve firing and produce vasopressor responses in rats.
Central hydrocortisone effects on sympathetic drive remain hypothesis-generating in rats; leaves open translation to human hypertension mechanisms.
Central effects of hydrocortisone were investigated by injecting it intracerebroventricularly (icv) while recording blood pressure and heart rate in awake rats. Dose-dependent increases in both blood pressure and heart rate occurred following injections of hydrocortisone. Pretreatment by icv injections of the angiotensin II antagonist, [Sar1-Ile8]angiotensin II, completely abolished vasopressor responses to subsequent injections of hydrocortisone. When rats were later anesthetized with urethan to allow recording of abdominal sympathetic nerve activity, hydrocortisone produced vasopressor responses accompanied by corresponding increases in sympathetic nerve firing, which were also abolished by central pretreatment with either [Sar1-Ile8]angiotensin II or angiotensin I converting-enzyme inhibitor, captopril. These results indicate that centrally administered hydrocortisone stimulates the brain renin-angiotensin system to produce vasopressor responses by increasing sympathetic nerve firing.
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Takahashi et al. (1983) studied this question.
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