Peripheral hypertonic saline, furosemide, and angiotensin II suppress vasoconstriction to acute stress in conscious rats.

Acute alterations in fluid volume elicit complex neurohumoral responses including activation of the sympathetic nervous system (SNS), renin‐angiotensin system and the release of vasopressin (AVP). We hypothesized that increased plasma osmolality, reduced plasma volume or direct stimulation of angiotensin receptors would suppress the initial stress‐induced increase in systemic vascular resistance (SVR) that results from activation of the SNS. We instrumented rats to measure mean arterial pressure (MAP), cardiac output, and heart rate. After recovery, ice cold water (1 cm deep) was rapidly added to a waterproof cage to startle conscious rats. Hyperosmolality was induced by hypertonic saline (HTS, 20% NaCl, 1 ml/kg iv). Volume depletion was caused by furosemide (10 mg/kg, sc). In addition, angiotensin II was infused (20 μg/kg/min) to directly activate angiotensin receptors. After pretreatment with HTS, furosemide, or angiotensin II, the increase in SVR during the initial startle response was attenuated. In rats pretreated with HTS or angiotensin II, the increase in MAP during the initial startle response was also attenuated. Our results demonstrated that HTS, furosemide, and angiotensin II suppress vasoconstriction in response to startle. This may be due to direct inhibition of the SNS, indirect inhibition from an increase in AVP release, or a combination of these effects. Supported by USPHS DA13256.