Responses of isolated and perfused dog coronary arteries to acetylcholine, norepinephrine, KCl, and diltiazem before and after removal of the endothelial cells by saponin. Left ventricular systolic performance during upright bicycle exercise in patients with essential hypertension. Rx drugs

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This study was undertaken to determine the effects of progesterone on the peripheral circulation. In prepubertal female pigs anesthetized with sodium pentobarbitone, changes in the superior mesenteric, left renal and left external iliac flow caused by intravenous infusion of progesterone were assessed using electromagnetic flow meters. Changes in heart rate and arterial blood pressure were prevented by atrial pacing and by connecting the arterial system to a pressurized reservoir containing Ringer solution. In 20 pigs, infusion of 1 mg/kg of progesterone increased mesenteric, renal and iliac flow. In a further 4 pigs, the vasodilatory effects of the hormone were enhanced by graded increases in the dose between 1, 2 and 3 mg/kg. The mechanisms of these responses were studied in the 20 pigs by repeating the experiment after hemodynamic variables had returned to the control values before infusion. In 5 pigs, blockade of adrenergic receptors with propranolol and phentolamine did not affect the responses elicited by progesterone. The increases in mesenteric, renal and iliac flow to progesterone were prevented, respectively, by the injection of N(omega)-nitro-L-arginine methyl ester into the mesenteric (5 pigs), the renal (5 pigs) or the iliac artery (5 pigs). The present study shows that intravenous infusion of progesterone dilated mesenteric, renal and iliac circulations. The mechanism of this response involved the release of nitric oxide. Copyright 2001 S. Karger AG, Basel

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Heart Vessels. 1986;2(4):221-7.
Responses of isolated and perfused dog coronary arteries to acetylcholine, norepinephrine, KCl, and diltiazem before and after removal of the endothelial cells by saponin.

Nakane T, Itoh N, Chiba S.

The vascular responses to acetylcholine (ACh), norepinephrine (NE), KCl, and diltiazem were examined before and after removal of endothelial cells by an intraluminal bolus injection of saponin (1 mg) in isolated and perfused dog coronary arteries. Without any precontraction, ACh induced a long-lasting vasodilation in small doses (less than 1 microgram), and an initial brief vasoconstriction was occasionally accompanied in large doses. These vascular responses to ACh were not significantly affected by the pretreatment with propranolol (5 X 10(-6) mol/l). The endothelial removal by intraluminal saponin was confirmed electron microscopically. After 20-60 min of saponin treatment, the responses to drugs were observed and compared with the control. The ACh-induced vasodilation was significantly attenuated by saponin (P less than 0.01), but the ACh-induced vasoconstriction was not affected by it. The vasodilation was blocked by atropine. The NE- and KCl-induced vasoconstrictions and diltiazem-induced vasodilation were not affected by saponin treatment. It is suggested that: (1) ACh produced a vasodilation in the nonpreconstricted condition of dog coronary arteries; (2) the vasodilation caused by ACh is mostly endothelium-dependent, which is considered to be mediated by muscarinic receptors; and (3) the vascular responses to NE, KCl, and diltiazem and the vasoconstriction produced by ACh are not influenced by removal of the endothelium in a relatively large epicardial coronary artery of the dog.

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Am J Med. 1983 Sep 26;75(3A):40-6.
Left ventricular systolic performance during upright bicycle exercise in patients with essential hypertension.

Francis CK, Cleman M, Berger HJ, Davies RA, Giles RW, Black HR, Vita N, Zito RA, Zaret BL.

Left ventricular performance was evaluated at rest and during maximal upright bicycle exercise in 51 patients with chronic essential hypertension. Twenty-eight of these patients had no clinical or electrocardiographic evidence of coronary artery disease and comprise the primary study population. The remaining 23 patients had coronary artery disease and represent a comparison group. First-pass radionuclide angiocardiograms were obtained at rest and during maximal upright bicycle exercise, allowing evaluation of global left ventricular ejection fraction and regional wall motion. At the time of the radionuclide studies, all patients were hypertensive, defined as a diastolic blood pressure 90 mm Hg or greater and/or a systolic blood pressure 140 mm Hg or greater with the patient at rest and sitting. In the primary study group, the left ventricular functional response to upright bicycle exercise was normal in 26 of 28 patients. Left ventricular ejection fraction averaged (+/- standard error) 65 +/- 2 percent at rest and increased significantly to 76 +/- 2 percent with exercise (p less than 0.001). Regional wall motion was normal both at rest and during exercise in all patients. Seventeen patients had electrocardiographic evidence of left ventricular hypertrophy, and 14 were receiving propranolol therapy. The left ventricular functional response also was normal in these subgroups. In contrast to the nearly uniform normal left ventricular responses noted in the patients with hypertension alone, the group with concomitant coronary artery disease had a markedly higher incidence of abnormal left ventricular reserve (19 of 23 versus two of 28, p less than 0.001) during exercise. Thus, in most patients with essential hypertension but without concomitant coronary artery disease, left ventricular reserve during exercise was normal. Hypertension, even with left ventricular hypertrophy, should not be viewed as the cause for an abnormal left ventricular response to exercise in a patient undergoing diagnostic exercise radionuclide angiocardiography.

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