Resting systolic, diastolic, and mean blood pressures (MBP), as well as heart rates, of unanesthetized, unrestrained, cold-acclimated (CA, 4 wk, 6 degrees C) rats were measured by direct arterial cannula and compared with those of controls maintained at 25 degrees C. Exposure to cold increased all these measurements significantly. Mean heart weight of CA rats was also increased significantly above that of controls. The responsiveness of MBP and heart rate to administration of the beta-adrenergic agonist, isoproterenol (3, 5, and 8 micrograms/kg ip), to unanesthetized, unrestrained, CA rats during exposure to air at 6 degrees C was similar to, and possibly less than, that of warm-acclimated (WA) rats measured at 25 degrees C. Acute administration of the alpha-adrenergic agonist, phenylephrine (100 micrograms/kg ip), to CA rats while in air at 6 degrees C induced less of a change in MBP from pretreatment level than was observed in WA rats. However, no differences were observed between groups when changes in heart rate from pretreatment level were compared. A similar statement may be made for a higher dose of phenylephrine (150 micrograms/kg ip), although MBP were elevated to higher levels in both groups with the higher dose. Abrupt exposure of WA rats to cold (6 degrees C) resulted in a sharp increase in heart rate and a more gradual increase in MBP over a period of 1 h. Removal of CA rats from 6 to 25 degrees C resulted in a gradual decrease in heart rate with no significant change in MBP during the ensuing hour.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies were performed on the ontogeny of arterial blood pressure and functional properties of the thoracic aorta in lean (L) and obese (O) male Zucker rats at ages of 6-36 wk. Body weight was larger in the O than the L at all ages, with differences reaching values of 200-250 g at ages over 24 wk (at 33-36 wk: L = 510 +/- 9 and O = 730 +/- 15 g). Systolic blood pressure was lower in young O compared with L (6-15 wk) but increased with age at a rate seven times greater in O than in L. For ages of 33-36 wk, systolic pressure was significantly higher in O compared with L (O = 132 +/- 2 vs. L = 122 +/- 2 mmHg). Total serum cholesterol (at 36 wk: L = 278 +/- 31 and O = 354 +/- 12 mg/dl) and triglycerides (at 36 wk: L = 493 +/- 71 and O = 1,618 +/- 220 mg/dl), as well as glucose levels, increased with age in both groups and were significantly higher in O at all ages. Serum levels of thyroxine but not triiodothyronine were significantly lower in O at all ages. No differences were found in passive mechanics at any age. Values of maximum active stress with smooth muscle activation by 75 mM K+ plus 10 microM norepinephrine were significantly higher at 24 and 36 wk in O (at 36 wk: L = 573 +/- 42 and O = 821 +/- 89 x 10(3) dyn/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

4 These changes appear unlikely to account completely for the antihypertensive effect of captopril because this compound has been shown to decrease blood pressure in hypertensive patients' and in experimental animals*" 8 with high, low, or normal plasma rcnin activity, as well as in the normotensive animal. 7 In addition, doses of captopril that lower blood pressure have been reported to have no effect on plasma bradykinin concentration.9 These findings have led many investigators"' '• 10 " u to question the in- hibition of angiotensin converting enzyme as the sole, or even the major, antihypertensive action of captopril. Another mechanism by which captopril could contribute to the reduction in blood pressure is by way of a direct action on arterial smooth muscle, which results in decreased vascular reactivity. The studies described here were designed to evaluate the effect(s) of acute administration of captopril on vascular reactivity of rat aortic rings to angiotensin I (AI), All, KG, norepinephrine, phenylephrine, isoproterenol, and bradykinin. The results of these studies suggest that captopril can exert an effect on vascular smooth muscle by reducing its responsiveness specifically to aadrenergic agonists. This decrease in vascular aadrenergic responsiveness may contribute to the antihypertensive action of captopril. Methods Tissue PreparationMale rats (Sprague-Dawley derived) weighing 420 to 540 g were used for this study. For each experiment, two rats were quickly guillotined and the thoracic aorta from each rat was rapidly excised and placed in a modified Krebs solution aerated with 95% O a : 5% COi.