Pulmonary vascular reactivity in the spontaneously hypertensive rat.
We examined the pulmonary vascular reactivity of normotensive rats (NR) and spontaneously hypertensive rats (SHR) to acute and chronic pressor stimuli. In rats kept at low altitude (1,520 m), SHR had a slight degree of right ventricular hypertrophy, but there was no difference between SHR and NR in either right ventricular systolic pressure or pulmonary artery wall thickness. When compared to blood-perfused lungs from low altitude NR, lungs from low altitude SHR were normoresponsive to acute airway hypoxia, hyporesponsive to intra-arterial angiotensin II, and hyperresponsive to intra-arterial prostaglandin F2alpha. After exposing rats to simulated high altitude (4--6 weeks at 4,270 m) to induce hypoxic pulmonary hypertension, SHR had a higher right ventricular systolic pressure, a greater degree of right ventricular hypertrophy, and more pulmonary artery medial thickening than did NR. The results indicate that although the pulmonary vasculature of SHR does not become hypertensive spontaneously, it might have an increased tendency to develop hypertension when exposed to an appropriate stimulus, i.e., chronic airway hypoxia.
D000531:Altitude; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D006332:Cardiomegaly / Q000209:etiology; D006321:Heart / Q000187:drug effects; D006400:Hematocrit; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D000860:Hypoxia / Q000150:complications; D008168:Lung / Q000098:blood supply*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D011460:Prostaglandins F / Q000494:pharmacology; D051381:Rats; D014655:Vascular Resistance / Q000187:drug effects
D011460:Prostaglandins F; D000804:Angiotensin II