Abstract-The initial stages of hypertension in the spontaneously hypertensive rat (SHR) are characterized by an increase in cardiac output. Venous capacitance plays an important role in the control of cardiac output. This study tested the hypothesis that venous tone is elevated in the developmental stages of spontaneous hypertension. Male SHR or normotensive Wistar-Kyoto (WKY) rats were instrumented for the measurement of arterial pressure (FAP) and intrathoracic vena caval pressure (FVP). A latex-tipped catheter was advanced into the right atrium via the jugular vein. Mean circulatory filling pressure (MCFP), an index of integrated venomotor tone, was calculated as MCFPϭFVPϩ(FAPϪFVP)/VAR. FAP and FVP were recorded after 5 seconds of right atrial balloon inflation. The venous to arterial compliance ratio (VAR) was estimated as 76 for WKY and 106 for SHR. Mean arterial pressure (MAP), heart rate, and MCFP were recorded in conscious rats of 4 to 6 and 8 to 10 weeks of age. In 4-to 6-week-old rats, both MAP and MCFP were significantly elevated in the SHR (MAP, 129Ϯ6 mm Hg; MCFP, 6.6Ϯ0.4 mm Hg) compared with the age-matched WKY (MAP, 91Ϯ6 mm Hg; MCFP, 5.4Ϯ0.4 mm Hg), whereas heart rate was not significantly different. The elevations in MAP (SHR, 144Ϯ4 mm Hg; WKY, 102Ϯ3 mm Hg) and MCFP (SHR, 7.7Ϯ0.3 mm Hg; WKY, 6.0Ϯ0.2 mm Hg) in SHR were exaggerated at 8 to 10 weeks of age. After ganglionic blockade (chlorisondamine; 10 mg/kg), the differences in MCFP were no longer statistically significant between SHR and WKY at both 4 to 6 weeks of age (3.9Ϯ0.2 versus 4.0Ϯ0.3 mm Hg) and 8 to 10 weeks of age (5.0Ϯ0.3 versus 4.3Ϯ0.3 mm Hg, respectively). The differences in MAP at 4 to 6 weeks of age (79Ϯ7 versus 67Ϯ5 mm Hg, respectively) also were not statistically significant after ganglionic blockade. However, a significant difference in MAP between strains remained after ganglionic blockade in 8-to 10-week-old rats (90Ϯ5 versus 63Ϯ3 mm Hg, respectively). These findings indicate that venous tone is increased via autonomic effector systems during the developmental stages of spontaneous hypertension. These data also suggest that autonomic mechanisms predominate at very early stages, whereas nonautonomic mechanisms assume more importance in maintaining the elevated MAP as hypertension progresses. (Hypertension. 1998;31[part 1]:139-144.)

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This study tested the hypothesis that acute psychological stress causes venoconstriction. Male Sprague-Dawley rats were instrumented with indwelling catheters in a femoral artery and vein and a balloon-tipped catheter in the right atrium. Mean arterial pressure (MAP), venous pressure, heart rate (HR), and mean circulatory filling pressure (MCFP) were monitored in conscious rats. Air-jet stress was performed before and after treatment with saline, chlorisondamine, phentolamine, or prazosin. Air-jet stress caused MAP, HR, and MCFP to increase by 10 +/- 1 mmHg, 31 +/- 4 beats/min, and 0.95 +/- 0.09 mmHg, respectively. Treatment with either chlorisondamine or phentolamine was equally effective in abolishing the stress-induced increases in MAP, HR, and MCFP. Prazosin treatment abolished the pressor response to air-jet stress but did not significantly affect the HR and MCFP responses. In contrast, pretreatment with the alpha 2-receptor antagonist rauwolscine hydrochloride abolished both the MAP and MCFP responses to air-jet stress but did not affect the HR response. These findings indicate that venoconstriction is an important component of the cardiovascular response to acute psychological stress. Stress-induced venoconstriction appears to be mediated primarily via the alpha 2-receptor subtype.

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