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At least 1,171 records · Page 65Linked to original sources
PubMed1987

Sympathetic function in spontaneously hypertensive rats after chronic administration of captopril.

The cardiovascular effects of electrical stimulation of the posterior hypothalamus, intravenous administration of norepinephrine (NE), and direct sympathetic nerve stimulation (SNS) were compared in spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY) given captopril (osmotic minipump, 1.25 micrograms/h icv) or vehicle for 4 wk beginning at age 7 wk. Mean arterial pressure (MAP) and renal and mesenteric flows (pulsed Doppler flow probes) were monitored in anesthetized rats. Following chronic administration of captopril the MAP was 141 +/- 4 mmHg in SHR receiving captopril and 183 +/- 6 mmHg in SHR receiving vehicle. Posterior hypothalamic stimulation, intravenous NE, and SNS resulted in lesser increases in MAP and renal and mesenteric vascular resistances in SHR treated with captopril. Response curves were shifted to the right, and the initial slopes and rate of change of slopes of the curves were less in captopril-treated SHR than vehicle-treated rats. The decrease in sensitivity to posterior hypothalamic stimulation was greater than the decrease in response to NE or SNS. The decrease in vascular reactivity in captopril-treated SHR was not due to increased sensitivity of the baroreflex for control of vascular resistance nor to a decrease in arterial pressure per se. WKY treated with captopril also showed lesser increases in MAP and renal and mesenteric vascular resistances in response to posterior hypothalamic stimulation, intravenous NE, and SNS. The depressor effects of intracerebroventricular captopril in SHR may be due, in part, to an attenuation in sympathetic vasoconstrictor tone. This attenuation involves both a decrease in vascular smooth muscle responsiveness to NE as well as a decrease in central stimulation of sympathetic outflow.

Animals↗
PubMed1996

Nitric oxide modulates arteriolar responses to increased sympathetic nerve activity.

The purpose of this study was to determine whether arteriolar responses to increased sympathetic nerve activity are limited by the actions of endogenous nitric oxide. Intravital microscopy was used to examine diameter responses of small feed arteries (SFA), first-order arterioles (1A) and second-order arterioles (2A) to perivascular sympathetic nerve stimulation in the superfused rat small intestine. Stimulation induced a frequency-dependent constriction in all vessel types that was completely abolished by the alpha-adrenoceptor antagonist phentolamine (10(-6) M). In SFA and 1A, the magnitude of sympathetic constriction was increased significantly in the presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine(L-NMMA, 10(-4) M). In SFA (n = 7), stimulation at 3, 8, and 16 Hz induced constrictions of 11 +/- 1, 28 +/- 4, and 42 +/- 3%, respectively, under the normal superfusate vs. 28 +/- 3, 46 +/- 5, and 76 +/- 3% in the presence of L-NMMA. For 1A (n = 7), stimulation induced constrictions of 10 +/- 1, 27 +/- 4, and 37 +/- 3% under the normal superfusate vs. 24 +/- 2, 47 +/- 3, and 72 +/- 4% in the presence of L-NMMA. The effect of L-NMMA on sympathetic constriction in SFA (n = 7) was completely reversed by the additional presence of 5 x 10(-3) M L-arginine in the superfusate. These results suggest that endogenous nitric oxide activity can attenuate sympathetic neurogenic constriction in the intestinal microvasculature.

Animals↗
PubMed1975

Ganglion cells in arterioles of skeletal muscle: role in sympathetic vasodilation.

Ganglion cells were found in arterioles of gracilis muscles of dogs 2 wk after complete extrinsic denervation. We tested the possibility that they function in active sympathetic vasodilation (SVD) induced in isolated gracilis muscles by hypothalamic stimulation. To this end various drugs were injected into the gracilis perfusate. (Drugs did not reach the systemic circulation, and exerted their effects within the gracilis itself). C6 had no effect. Submaximal doses of atropine or l-hyoscyamine delayed and slowed SVD; higher doses blocked completely. d-Hyoscyamine did not change SVD or acetylcholine vasodilation, but when administered prior to l-hyoscyamine, threshold for blockade of SVD by the l-isomer increased 10,000-fold. Blockade by l-hyoscyamine of acetylcholine vasodilation was unaltered by d-hyoscyamine. Eserine partly blocked SVD, but enhanced and prolonged acetylcholine vasodilation. The foregoing and certain features of the time course of SVD are interpreted to mean that: a) atropine blocks SVD at muscarinic sites on peripheral ganglion cells; b) transmission at the ganglion cells depends on slow excitatory postsynaptic potentials; c) the final mediator of SVD at the vascular muscle cell is unknown.

Acetylcholine↗
PubMed1976

Influence of sympathetic nerves on oxygen uptake or resting mammalian skeletal muscle,.

Gracilis muscles of anesthetized dogs were isolated and perfused with blood at constant flow. Oxygen uptake (Vo2) was measured by spectrophotometry of paired arterial and venous samples and monitored by continuous recording of HbO2 saturation. The sympathetic chain, connected to the isolated muscles, was stimulated electrically with supramaximal pulses. High frequencies (8-16/s) increased vascular resistance (R, ratio to control 1.86 +/- 0.6 SEM) and decreased Vo2 (0.61 +/- 0.02). Both effects could be maintained 10 min or longer. After stimulation there was an increase in Vo2, which could be less than equal to, or greater than the O2 deficit, depending on the stimulation frequency, the period of stimulation, and the blood flow. Low frequencies (0.5-4/s) increased R (1.39 +/- 0.04) and increased Vo2 during (1,18 +/- 0.03) and after stimulation. In several experiments there was an initial decrease in Vo2 which changed to an increase during the stimulation period while R remained elevated. These observations indicate that the decrease in Vo2 is due to closure of precapillary sphincters, whereas the increase is a direct effect on cell metabolism.

Animals↗
PubMed2003

Alpha-adrenergic vascular responsiveness to sympathetic nerve activity is intact after head-down bed rest in humans.

Space-flight and its ground-based simulation model, 6 degrees head-down bed rest (HDBR), cause cardiovascular deconditioning in humans. Because sympathetic vasoconstriction plays a very important role in circulation, we examined whether HDBR impairs alpha-adrenergic vascular responsiveness to sympathetic nerve activity. We subjected eight healthy volunteers to 14 days of HDBR and before and after HDBR measured calf muscle sympathetic nerve activity (MSNA; microneurography) and calf blood flow (venous occlusion plethysmography) during sympathoexcitatory stimulation (rhythmic handgrip exercise). HDBR did not change the increase in total MSNA (P = 0.97) or the decrease in calf vascular conductance (P = 0.32) during exercise, but it did augment the increase in calf vascular resistance (P = 0.0011). HDBR augmented the transduction gain from total MSNA into calf vascular resistance, assessed as the least squares linear regression slope of vascular resistance on total MSNA (0.05 +/- 0.02 before HDBR, 0.20 +/- 0.06 U.min-1.burst-1 after HDBR, P = 0.0075), but did not change the transduction gain into calf vascular conductance (P = 0.41). Our data indicate that alpha-adrenergic vascular responsiveness to sympathetic nerve activity is preserved in the supine position after HDBR in humans.

Adult↗
PubMed1986

Nucleus paragigantocellularis lateralis and lumbar sympathetic discharge in the rat.

Two classes of medullospinal units with inhibitory baroreceptor inputs [nucleus paragigantocellularis lateralis (PGCL) units] were recorded in PGCL (conduction velocity 3.1 and 0.67 m/s, respectively). Single-pulse stimulation of PGCL produced two peaks of activation of the lumbar sympathetic chain [sympathetic nerve discharge (SND)] with latencies of 98 and 206 ms. After substracting the delay due to impulse propagation between cord and sympathetic chain (64 ms), a conduction velocity of 2.8 and 0.67 m/s could be estimated for the medullospinal portion of the two sympathoexcitatory pathways stimulated in the PGCL. R wave-triggered activity histograms of PGCL unit discharge and lumbar SND exhibited a similar pattern with one major trough, occurring 108 ms later at the level of the sympathetic chain. It is concluded that PGCL contains two classes of medullospinal neurons with sympathoexcitatory function, the fast-conducting type being predominantly responsible for the cardiac-related rhythm of lumbar SND. Finally, averaging techniques revealed a large respiratory rhythm of lumbar SND in spontaneously breathing rats, but little or no such rhythm could be detected at the level of most PGCL sympathoexcitatory cells.

Animals↗