Hypoxic pulmonary vasoconstriction in blood-perfused isolated dog lungs progressively diminishes with repeated hypoxic challenges. We investigated the role of prostaglandins in effecting the decay of the hypoxic response by using a double perfusion preparation that could separately perfuse the right and left lungs of a single dog. Degeneration of this response was reversed by the addition of prostaglandin (PG) synthesis inhibitors, aspirin, or indomethacin. Various PG's known to be produced by the lung (PGE1, PGE2, and PGF2alpha), were infused, and only PGE1 abolished hypoxic pulmonary vasoconstriction. Since other workers have shown that lungs can synthesize and release PG's in response to various stimuli, we postulate that PGE1 synthesis in isolated lungs may increase and thereby cause the degeneration of the hypoxic response. The addition of aspirin or indomethacin could inhibit the synthesis of PGE1 and thereby restore hypoxic pulmonary vasoconstriction.
SUMMARY This study examines the influence of dopamine on plasma catecholamine, prolactin (PRL), and mean arterial pressure (MAP) responses to upright posture and isometric handgrip exercise and the recumbent circadian PRL and MAP patterns in essential hypertension. Nine men with sustained essential hypertension and nine age-and weight-matched normotensive controls were studied after they had reached metabolic equilibrium on a constant intake of 100 mEq sodium and 80 mEq potassium. The hypertensive group, but not the normotensive group, displayed a PRL response to upright posture and isometric handgrip. Hypertensives and normotensives had similar basal supine catecholamine levels and similar epinephrine and dopamine responses to posture and handgrip. The hypertensives had greater (p < 0.01) norepinephrine (NE) responses to posture and handgrip than did the normotensives. Bromocriptine (BEC) depressed supine basal MAP in the hypertensives but not in the normotensives. BEC markedly decreased the basal PRL levels in both groups. BEC eliminated the PRL response to posture in the hypertensives and depressed the NE response to posture and handgrip to a greater extent (p < 0.01) in the hypertensives than in the normotensives. In the control period, a clear circadian rhythm of PRL and MAP was noted in both groups. In both groups an increase in PRL concentration occurred between 60 to 90 minutes after sleep onset, and was followed by several larger secretory episodes resulting in progressively higher levels during the night with peak values occurring at the end of the sleep period, generally at 0500 to 0600 hours. During the hour after awakening, a fall in PRL concentration began, and lowest levels were reached at approximately 1100 hours in both groups. The mean 24-hour PRL levels in the hypertensive group (12.6 ± 0.5 ng/ml) were higher (p < 0.01) than in the normotensives ( 13 Accordingly, any stimulation of TIDA activity reduces PRL secretion from pituitary lactotropes and mechanisms leading to decreased tuberoinfundibularneuronal secretion of dopamine (DA) increase PRL secretion. Evidence has accumulated that this PRLregulating mechanism may also participate in blood
The effects of infused angiotensin on hypoxic pulmonary vasoconstriction in blood-perfused isolated dog lungs were studied. By using a double-perfusion system we were able to perfuse the right and left lungs separately in the same animal; one lung was used as control and the other lung was experimentally modified. The vasoconstrictive response to hypoxia decreased with time in the isolated lung preparations. The infusion of either angiotensin I or angiotensin II (1.2-5.8 mug/min) caused a threefold increase in the vasoconstrictive response to hypoxia over control levels. A second hypoxic period during the infusion usually yielded a diminished response, suggesting further degeneration of the response irreversible with angiotensin. It was concluded that angiotensin I or angiotensin II temporarily enhances hypoxic pulmonary vasoconstriction in isolated dog lungs.
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