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Vasodilator responses following intracranial stimulation of the trigeminal, facial and glossopharyngeal nerves in the cat gingiva.

The effects of electrical stimulation of the trigeminal, facial and glossopharyngeal nerves on gingival blood flow in the cat were studied. The intracranial part of these nerves was stimulated electrically, and gingival blood flow was measured by the laser Doppler technique. Electrical stimulation of the trigeminal, facial and glossopharyngeal nerves caused blood flow to increase in the ipsilateral gingiva both with the cranial nerve intact and after cutting it to the medulla. Stimulation of the distal cut ends of the facial and glossopharyngeal nerves elicited an increase in blood flow but no increase in systemic blood pressure. Pretreatment with hexamethonium reduced the increase in blood flow elicited by electrical stimulation of the facial and glossopharyngeal nerves, but had no effect on that elicited by stimulation of the trigeminal nerve. In contrast, pretreatment with tripelennamine attenuated the trigeminal nerve-stimulated blood flow increase, but not that elicited by stimulation of the facial and glossopharyngeal nerves. Atropine, propranolol and phentolamine had no effect on these responses. These results suggest that the autonomic nervous system, particularly the parasympathetic nervous system, is responsible for the blood flow increase elicited by facial and glossopharyngeal nerve stimulation, and that the trigeminal nerve-stimulated blood flow increase is induced by antidromic vasodilatation of the trigeminal sensory nerve.

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Capsaicin-sensitive nonadrenergic and noncholinergic depressor response to spinal cord stimulation in the pithed rat.

The effects of capsaicin on nonadrenergic, noncholinergic depressor responses to spinal cord stimulation were studied in pithed rats. Mean blood pressure (MBP was maintained at a level of 100 mmHg by continuous infusion of methoxamine and hexamethonium to block autonomic outflow. Electrical stimulation of the lower thoracic region (T9-12) via a pithing rod produced a frequency (1-8 Hz)-dependent fall in elevated MBP. The depressor response was abolished by tetrodotoxin, whereas atropine, propranolol, and cimetidine plus pyrilamine did not affect the response. Capsaicin treatment abolished the depressor response. These results suggest that spinal cord stimulation causes neurogenic vasodilation which is mediated by capsaicin-sensitive nonadrenergic and noncholinergic vasodilator nerves.

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Intrathecal administration of non-NMDA receptor agonists increases arterial pressure and heart rate in the rat.

We have found that spinal NMDA receptors are involved in control of sympathetic output in pathways to the heart and vessels. The present study was done to determine whether spinal non-NMDA excitatory amino acid receptors participate in cardiovascular regulation. Experiments were done on urethane-anesthetized Sprague-Dawley rats, giving the non-NMDA receptor agonists, quisqualate and kainate, and the antagonist, kynurenate, intrathecally at the spinal T9 level. Both quisqualate (30 nmol; n = 7; to activate AMPA receptors) and kainate (2 nmol; n = 6; to activate K receptors) increased arterial pressure and heart rate. The responses were characterized by a rapid onset, achieving, in most cases, greater than 80% of the maximum response within 1-4 min, and a persistence throughout the remaining 20-24 min of the experiment. I.v. injection of hexamethonium (10 mg/kg) prevented the effects of intrathecal administration of quisqualate (n = 5) but not of kainate (n = 7). To determine whether the hexamethonium-resistant effects of kainate were due to a peripheral action, kainate was given i.v. (n = 6); it was found to be without effect on arterial pressure or heart rate. The increases in arterial pressure and heart rate produced by intrathecal administration of quisqualate (30 nmol; n = 6), kainate (2 nmol; n = 6), glutamate (1 mumol; n = 6) and NMDA (2 nmol; n = 6) but not carbachol (27.4 nmol; n = 6) were prevented by similar preadministration of kynurenate (125 nmol). Intrathecal administration of kynurenate (125 nmol; n = 6; 500 nmol; n = 7) decreased arterial pressure and/or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

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Contribution of the central interaction between calcium and sodium to hemodynamic regulation in spontaneously hypertensive rats.

The contribution of the central interaction between calcium and sodium to hemodynamic regulation was assessed in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats. The effect of a high calcium solution (Ca2+, 130 mg/dl, 10 microliters) infused into the cerebral ventricle (i.c.v.) on hemodynamic responses induced by a high sodium solution (Na+, 1,000 mEq/1, 10 microliters) i.c.v. and the mechanism by which high Ca2+ affects the hemodynamic responses induced by high Na+ i.c.v. were studied. High Na+ i.c.v. induced a pressor response with tachycardia in the SHRs, but induced a pressor response with reflex bradycardia in the WKYs. Prior treatment with high Ca2+ i.c.v. attenuated the pressor response induced by high Na+ i.c.v. (+55.6 +/- 4.4 to +33.1 +/- 3.2 mmHg, P < 0.01) and restored reflex bradycardia (+86.4 +/- 7.7 to -26.7 +/- 7.6 bpm, P < 0.01) in SHRs. Whereas prior treatment with high Ca2+ i.c.v. attenuated the pressor response (+35.7 +/- 2.0 to +22.2 +/- 4.0 mmHg, P < 0.05), it did not alter the degree of reflex bradycardia (-81.7 +/- 7.1 to -69.2 +/- 120 bpm, n.s.) in WKYs. Ganglionic blockade attenuated the pressor response (+56.9 +/- 3.5 to +42.9 +/- 2.3 mmHg, P < 0.05) and restored reflex bradycardia (+82.1 +/- 10.3 to -65.9 +/- 11.0 bpm, P < 0.01) in SHRs, whereas, inhibition of arginine vasopressin attenuated the pressor response without modification of the tachycardic response.(ABSTRACT TRUNCATED AT 250 WORDS)

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