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Biomedical subjects

F N Miller

Publications and source records attributed to F N Miller.

119 records · Page 7Linked to original sources
PubMedDate not supplied

Met-enkephalin-induced vasoconstriction in the microcirculation of rat striated muscle.

Sprague-Dawley rats were anesthetized with pentobarbital (50 mg/kg) and the arterioles of the cremaster muscle were observed using television microscopy. Methionine (Met)-enkephalin was added to give bath concentrations of 10(-11) to 10(-7) M. Met-enkephalin caused a decrease in the diameter of first-order (127 +/- 7 microns), second-order (57 +/- 7 microns), and third-order (18 +/- 2 microns) arterioles, with the third-order arterioles showing the greatest reactivity. The effects of Met-enkephalin were attenuated by the opiate antagonist, naloxone, by the alpha-adrenergic receptor antagonists, phentolamine and prazosin, and by chemical sympathectomy with 6-hydroxydopamine. These results suggest that Met-enkephalin causes vasoconstriction in the striated muscle microcirculation by stimulating norepinephrine release from local nerve terminals.

Animals↗
PubMedDate not supplied

L-arginine restores cholesterol-attenuated microvascular responses in the rat cremaster.

The role of L-arginine in the reversal of cholesterol-induced endothelial dysfunction was studied in the cremaster muscle microcirculation. In vivo television microscopy was used to measure microvascular diameters and macromolecular leakage. Male Sprague-Dawley rats were fed either a normal chow diet or a diet supplemented with 1% cholesterol and 0.5% cholic acid for 3 weeks prior to in vivo experimentation. The cholesterol diet caused a decreased third-order arteriole dilator response to both acetylcholine and serotonin. This decreased responsiveness occurred in the presence of a higher plasma concentration of L-arginine and an increased ratio of L-arginine to its metabolite L-citrulline. The attenuation to both agonists was reversed by intravenous infusion of the nitric oxide precursor L-arginine (30-mg/kg bolus and 10-mg/kg/min continuous infusion). The cholesterol diet also decreased the postcapillary macromolecular leakage response to serotonin, and again this effect was reversed by L-arginine infusion. D-Arginine infusion had no restorative effect with either agonist in the cholesterol animals. Further experimentation with the nitric oxide production inhibitor N omega-nitro-L-arginine methyl ester demonstrated an inhibition of aretriolar dilation to acetylcholine, but there was no inhibition of dilation or macromolecular leakage to serotonin. Thus, it is probable that serotonin-induced leakage as well as dilation was not caused by stimulation of nitric oxide. These results suggest that L-arginine restores both nitric oxide-dependent and -independent dilation as well as macromolecular leakage in cholesterol-fed rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMedDate not supplied

Comparison of early microcirculatory and aortic changes in hypercholesterolemic rats.

The microcirculatory changes caused by hypercholesterolemia were studied in the rat cremaster muscle model by intravital microscopy and were compared with aortic ring segments from the same animals. Male Sprague-Dawley rats were fed either a normal chow diet or a chow diet supplemented with 1% cholesterol and 0.5% cholic acid for 3 or 5 weeks before experimentation. Three weeks of hypercholesterolemia produced a significantly decreased vasodilator response to serotonin in the arterioles. This response was also seen after 5 weeks on the hypercholesterolemia diet. Three weeks of hypercholesterolemia produced a significantly increased macromolecular leakage from postcapillary venules in response to serotonin. However, after 5 weeks of hypercholesterolemia, the serotonin-induced leakage was less than in control animals. Hypercholesterolemia for 3 weeks decreased the arteriolar dilation evoked by acetylcholine but did not change the arteriolar response to sodium nitroprusside. Contraction of the aortic rings induced by serotonin and aortic ring relaxation induced by sodium nitroprusside were not different between 3-week-control and 3-week-hypercholesterolemic animals. However, 3 weeks of hypercholesterolemia attenuated the aortic ring relaxation evoked by acetylcholine. These results suggest that hypercholesterolemia causes an early depression of endothelium-derived relaxing factor (EDRF)-mediated receptor responses in both microvessels and the aorta, whereas non-EDRF-mediated receptor responses are altered in the microcirculation but not in the aorta.

Acetylcholine↗
PubMedDate not supplied

Progressive microvascular alterations with the development of renovascular hypertension.

Norepinephrine-induced changes in diameters of first- (1A), second- (2A), and third-order (3A) arterioles in the exposed cremaster muscles of normotensive and renovascular hypertensive rats were quantitated via television microscopy. By 2 weeks following the surgery to induce hypertension, we found that 3A sensitivity to norepinephrine had increased and the 1As had chronically constricted. By 4 weeks, the constriction had progressed to include both 1A and 2A. Sensitivity was no longer increased in 3As and, in fact, sensitivity had decreased in 1As and 2As. The 1As and 2As could not be dilated with isoproterenol or nitroprusside; thus, the vessels appeared to have undergone a structural alteration. We suggest from these results that the early increased 3A sensitivity contributes to the initial development of hypertension. The larger arterioles then constrict to protect the downstream vessels from increased luminal pressure. As the hypertension develops, the constriction progresses to smaller arterioles in an attempt to maintain normal pressure in the capillaries (site of water exchange). The constricted arterioles contribute to increased total peripheral resistance, and with the constriction, there occurs a general decrease in vessel responsiveness.

Abdomen↗