Electrical stimulation in perifornical lateral hypothalamus decreases coronary blood flow in cats

Based on evidence implicating the central nervous system in the regulation of coronary vascular resistance and the knowledge that the hypothalamus is a central site for integration of cardiovascular control, studies were undertaken to determine if electrical stimulation in the hypothalamus produced coronary vasoconstriction. In anesthetized cats, following beta-adrenergic receptor blockade, stimulation in perifornical lateral hypothalamus produced a transient decrease in coronary blood flow velocity (30 +/- 5%), a small pressor effect (7 +/- 2 mmHg), and an initial decrease in hindquarter blood flow velocity (51 +/- 5%). The decrease in coronary flow velocity, which had an onset latency of 1-3 s and a duration of 5-15 s, was abolished by ipsilateral stellate ganglionectomy and by intravenous and intracoronary prazosin. The coronary vasoconstriction produced by hypothalamic stimulation was not different from that produced by cardioaccelerator nerve stimulation. These results suggest that electrical stimulation of a hypothalamic site produces an alpha-adrenergic receptor-mediated decrease in coronary blood flow that is unmasked by beta-adrenergic receptor blockade, requires the integrity of ipsilateral cardiac sympathetic innervation, and mimics the coronary response to cardioaccelerator nerve stimulation.

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Activation in the region of parabrachial nucleus elicits neurogenically mediated coronary vasoconstriction

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.5.h1585 ◽

1991 ◽

Vol 261 (5) ◽

pp. H1585-H1596 ◽

Cited By ~ 2

Author(s):

F. J. Miller ◽

M. L. Marcus ◽

M. J. Brody ◽

D. D. Gutterman

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Electrical Stimulation ◽

Arterial Pressure ◽

Flow Velocity ◽

Blood Flow Velocity ◽

Chemical Activation ◽

Parabrachial Nucleus ◽

Coronary Vasoconstriction ◽

Coronary Blood Flow Velocity

A role for parabrachial nucleus in cardiovascular regulation is suggested by evidence that electrical stimulation in this region elicits increase in heart rate and arterial pressure. We hypothesized that parabrachial nucleus may also be involved in control of coronary vasomotor tone. After beta-adrenergic receptor blockade in anesthetized cats, electrical stimulation in the region of parabrachial nucleus produced no change in heart rate, an increase in arterial pressure (34 +/- 6 mmHg), and a transient reduction in coronary blood flow velocity (-21 +/- 2%). Coronary resistance (72 +/- 9%) and femoral resistance (189 +/- 31%) increased markedly. The decrease in coronary blood flow velocity was abolished by stellate ganglionectomy or alpha 1-adrenergic blockade without altering pressor or femoral responses. Injection of the neurotransmitter L-glutamate or kainic acid into parabrachial nucleus also elicited coronary vasoconstriction. We conclude that electrical or chemical activation in the region of parabrachial nucleus elicits coronary vasoconstriction as part of a generalized sympathetic activation. The fact that the coronary response is elicited by chemical activation suggests that cell bodies in the region of medial parabrachial nucleus and subceruleus, as opposed to fibers of passage, are involved in this central neural coronary vasoconstriction.

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Daily exercise enhances coronary resistance vessel sensitivity to pharmacological activation

Journal of Applied Physiology ◽

10.1152/jappl.1989.66.1.421 ◽

1989 ◽

Vol 66 (1) ◽

pp. 421-428 ◽

Cited By ~ 37

Author(s):

S. E. DiCarlo ◽

R. W. Blair ◽

V. S. Bishop ◽

H. L. Stone

Keyword(s):

Blood Flow ◽

Flow Velocity ◽

Coronary Blood Flow ◽

Blood Flow Velocity ◽

Adrenergic Receptor ◽

Coronary Resistance ◽

Pharmacological Agents ◽

Daily Exercise ◽

Vascular Sensitivity ◽

Coronary Blood Flow Velocity

The effect of daily exercise on the coronary resistance vessel sensitivity to intracoronary infusion of several pharmacological agents was assessed in 12 conscious adult mongrel dogs. alpha-Adrenergic receptor agonists (norepinephrine and phenylephrine) significantly decreased coronary blood flow velocity. beta 2-Adrenergic receptor agonists (isoproterenol and zinterol) and a metabolic vasodilator (adenosine) significantly increased coronary blood flow velocity. These responses occurred without altering factors that influence myocardial metabolism. Daily exercise significantly enhanced the coronary vascular sensitivity to each of the pharmacological agents. These results suggest that a nonspecific potentiation to pharmacological activation occurs after daily exercise. After left stellate ganglionectomy, intracoronary infusions of each pharmacological agent had similar effects on coronary blood flow velocity as presented for the intact dogs; however, daily exercise did not enhance the coronary vascular sensitivity to the pharmacological agents. These results demonstrate the need for an intact nervous system for the vascular adaptations associated with daily exercise.

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