The renin-angiotensin system of uninephrectomized rats under diuretic treatment.
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Angiotensin II↗
Biomedical subjects
D Susic
Publications and source records attributed to D Susic.
Heparin lowers the blood pressure in hypertensive rats.
This study describes the effect of heparin on blood pressure, cardiac output, and total peripheral resistance in spontaneously hypertensive and one-kidney, one clip Goldblatt hypertensive rats. Administration of heparin (200 units/day/rat) for 8 weeks to young (6-week-old) spontaneously hypertensive rats (SHR) resulted in an attenuated rise in blood pressure; mean blood pressure in heparin-treated SHR (180 +/- mm Hg) was significantly lower (p less than 0.05) than that in control SHR (205 +/- 7 mm Hg). Similar heparin treatment started immediately after the induction of one-kidney, one clip (Goldblatt) hypertension reduced the rise in blood pressure. After 4 weeks of treatment, heparin-treated Goldblatt hypertensive rats had much lower blood pressure (150 +/- 4 mm Hg) than did control rats (7178 +/- 8 mm Hg). The difference was highly significant (p less than 0.01). Similarly, heparin treatment also lowered the blood pressure in rats with developed Goldblatt hypertension. After the cessation of heparin treatment, the blood pressure returned to pretreatment level in these rats. When compared to vehicle-treated rats, heparin-treated animals with either spontaneous or Goldblatt hypertension concomitantly exhibited a significant increase in cardiac output, and significant decreases in total peripheral resistance and packed cell volume. Further, the left ventricular weight to body weight ratio was significantly lower (p less than 0.05) in heparin-treated than control animals. Since a relationship seems to exist between an increase in packed cell volume and blood viscosity and the rise in arterial pressure, this blood-pressure-lowering effect of heparin may be attributed to a decrease in packed cell volume.
Animals↗
Hemodynamic effects of chronic alteration in hematocrit in spontaneously hypertensive rats.
This study describes the effect of a chronic decrease in hematocrit on blood pressure, cardiac output (CO), total peripheral resistance (TPR), and plasma volume in spontaneously hypertensive rats (SHR), and all but plasma volume in normotensive Wistar rats (NWR). Hematocrit was decreased by treatment with either heparin, vitamin K inhibitor ( pelentan ), or by repeated blood letting (BL). The results show that in SHR, a decrease in hematocrit, regardless of how produced, was associated with a significant decrease (p less than 0.01) in blood pressure. Prevention of heparin-induced decrease in hematocrit by repeated transfusions of red blood cells abolished the blood-pressure-lowering effect of heparin. By using combined data on hematocrit and systolic blood pressure in all five SHR groups, a significantly positive correlation and linear regression between hematocrit and blood pressure were obtained. When compared to control untreated SHR, heparin- or pelentan -treated SHR showed a significant (p less than 0.001) decrease in TPR and a significant increase in CO, while in SHR BL, no difference in TPR or CO was found. Plasma or blood volume did not differ among the groups. In NWR, heparin treatment resulted in significantly decreased hematocrit, decreased TPR, and increased CO compared to control normotensive rats. However, blood pressure did not change. Results confirming the authors' previous study and those of other investigators indicate a direct association between hematocrit and systemic hypertension. Lowering the hematocrit can effectively lower an elevated blood pressure. Moreover, the data suggest that heparin or pelentan induces a vasodilator effect that cannot be attributed to a decrease in hematocrit alone.
Animals↗