Streptozotocin-induced diabetes mellitus lowers blood pressure in spontaneously hypertensive rat.

There are conflicting reports showing that alloxan or streptozotocin-induced diabetes in rat increases, decreases or does not alter blood pressure. Since hypertension influences organ-specific diabetic complications, this study was designed to examine the effects of streptozotocin-induced diabetes on blood pressure (BP), hemodynamics and heart weight in spontaneously hypertensive (SHR) and normotensive Wistar (NWR) rats. In order to control the influence of weight loss on BP affected by diabetes, we have examined the effect of weight loss without diabetes on BP, hemodynamics and heart weight in SHR. Weight loss parallel to that in diabetic SHR was induced in a group of SHR by food restriction (fasting). Significant (P less than .05) decreases in systolic and direct BP were observed in diabetic SHR. This hypotensive effect was accompanied by a significant (P less than .05) decrease in total peripheral resistance, but no change in cardiac output. These blood pressure and hemodynamic findings in diabetic SHR were complimented by a significant (P less than .05) reduction in left ventricular weight to body weight ratio. On the contrary, fasting SHR with weight loss equivalent to that in diabetic SHR showed no change in BP or total peripheral resistance. Further, fasting SHR revealed a significant (P less than .05) increase in heart weight to body weight ratio. The weight loss of equal magnitude induced by streptozotocin-induced diabetes in NWR did not have any effect on BP or hemodynamics. In addition, like fasting SHR, diabetic NWR showed a significant (P less than .05) increase in left ventricular weight to body weight ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin synthesis inhibitors potentiate the antihypertensive effect of heparin in spontaneously hypertensive rats.

We have shown that heparin lowers blood pressure significantly in hypertensive rats. This study was initiated to examine whether prostaglandin (PG) mediates the antihypertensive action of heparin. To this end, the effect of three different PG synthesis inhibitors (indomethacin, aspirin, meclofenamate) on the cardiovascular and renal actions of heparin was studied in spontaneously hypertensive rats (SHR). During 4 weeks of treatment, heparin reduced blood pressure significantly (P less than 0.01) in SHR. This was accompanied by significant decrements in hematocrit and total peripheral resistance but a significant increment in cardiac output. All of the PG inhibitors used significantly potentiated the antihypertensive effect of heparin and further reduced blood pressure by about 20%. Although heparin alone increased plasma renin activity, heparin and PG inhibitors together prevented this effect. When compared with heparin-treated rats, SHR treated with heparin and PG inhibitors combined had significantly (p less than 0.05 to 0.01) lower plasma aldosterone levels. These levels, however, were not different from SHR treated with PG inhibitors alone. Like blood pressures, the renal histopathologic lesions in SHR treated with heparin or heparin and PG inhibitors combined were significantly less severe than those in untreated SHR or SHR treated with PG inhibitors alone. Finally, captopril was shown to potentiate the effect of heparin. In conclusion, the antihypertensive effect of heparin does not appear to be PG mediated, but may be related to the structural changes in renal arterioles, inhibition of angiotensin-converting enzyme, or both.