Pulmonary vasoactivity of several biochemical components produced or stored in platelet was the justification for the study of pulmonary artery pressure in fawn-hooded rats (FHR) with hereditary platelet storage pool deficiency. Anesthetized (pentobarbital 35 mg kg-1 i.p.) FHR had higher right ventricular systolic pressure compared with normal Wistar rats (NWR) matched in sex and age (57.7 ± 6,8 vs. 34.8 ± 1.2 mm Hg; p < 0.01). The incidence of higher pulmonary artery pressure ( > x + 2 SD of NWR) was 68% among FHR. A significant difference was recorded between FHR and NWR in the relative weight of the right ventricle (0.092 ± 0.021 vs. 0.048 ± 0.001 g/100 g; p < 0.05). Rise in pulmonary artery pressure in FHR after 4 weeks of normobaric hypoxia was found to be comparable to that seen posthypoxically in NWR. Morphological consequences of pulmonary hypertension, ranging from moderate medial hypertrophy of small arteries to muscularization of pulmonary arterioles, were recorded in about 50% of FHR with increased pulmonary artery pressure
SUMMARY 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 < 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, heparintreated Goldblatt hypertensive rats had much lower blood pressure (150 ± 4 mm Hg) than did control rats (178 ± 8 mm Hg). The difference was highly significant (p < 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 < 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. (Hypertension 4: 681-685, 1982) KEY WORDS * spontaneous hypertension • one-kidney, one clip hypertension cardiac output • peripheral resistance • packed cell volume (hematocrit) A LTHOUGH heparin has been known for a long time, reports on its cardiovascular effects are Lscarce. Mandal et al.1 have reported that prolonged heparin treatment normalizes the blood pressure in young and old spontaneously hypertensive rats (SHR), but no information with regard to cardiovascular hemodynamics was available from this work. The study of Wilson et al., 2 despite some differences, has essentially confirmed these results, since they found that chronic administration of heparin attenuates the rate of rise in systolic blood pressure and prevents severe fibrinoid vascular lesions in stroke-prone SHR. Heparin also has been found to inhibit rat arterial smooth muscle cell proliferation in vivo and in vitro, a finding that suggests a possible effect of heparin on total peripheral resistance and therefore on blood pressure.All these data prompted us to initiate further investigation of the hemodynamic effects of heparin. To this end, the effects of heparin on blood pressure, cardiac output, and total peripheral resistance was examined in SHR and rats with one-kidney, one clip Goldblatt hypertension. Materials and MethodsTwo different models of hypertension i...
Rats made hypoxic by confinement in hypoxic cages for 4 weeks developed pulmonary hypertension and right ventricular hypertrophy. Treatment with Verapamil® or aspirin reduced both chronic hypoxic pulmonary hypertension and the hypertrophy of the right ventricle. The antihypertensive effect of Verapamil is explained by the involvement of the transmembrane calcium flux in pulmonary vascular smooth muscle in the hypoxic vasoconstrictory response. Part of the antihypertensive effect of inhibition of prostaglandin synthesis is attributed to a decrease in packed cell volume produced in hypoxic, aspirin-treated rats.
Treatment with SQ 14.225, an inhibitor of the enzyme converting angiotensin I to angiotensin II and lowering of plasma renin activity by dietary salt overload, significantly decreased hypertrophy of the right ventricle in chronically hypoxic rats. The smaller degree of right ventricular hypertrophy registered in hypoxic rats with suppressed activity of the renin-angiotensin system was proportional to the decrease in hypoxic pulmonary hypertension noted in these animals. Lowering of pulmonary hypertension in chronically hypoxic rats by suppression of the renin-angiotensin system is consistent with the idea that angiotensin II may be involved in eliciting hypoxic pulmonary vasoconstriction. Inhibition of converting enzyme also lowered the systemic arterial pressure in hypoxic rats, but this finding could not be taken as evidence for the role of the renin-angiotensin system in homeostatic control of blood pressure in normal animals, since the plasma-renin activity in hypoxic rats is increased and the blood pressure higher than in rats kept under normoxic conditions.
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