Circulatory Dynamics in Spontaneous and Nephrogenic Hypertensive Dogs during the Depressor Response to Acute Inflammation

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Abstract
Cardiac output and blood voluine are at control levels in unanesthetized hypertensive dogs during the depressor response to acute inflammation. Hence the fall in blood pressure is due to a decreased total peripheral resistance. The accompanying renal hyperemia indicates that decreased resistance in the renal vascular bed accounts for a significant portion of the fall in total peripheral resistance. Drug studies further suggest that acute inflammation operates to lower blood pressure in hypertensive dogs via mechanisms other than complete paralysis of autonomic vasomotor activity.