Diencephalic vasodepressor responses independent of heart rate changes

Kristt, Donald A.

doi:10.1016/0024-3205(75)90260-x

Cited by 7 publications

(2 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Unlike most other hypothalamic areas which are predominantly pressor, the anterior hypothalamus lowers blood pressure when it is stimulated electri-Miyajima and Bu/iag/Hypothalamic Inhibition by Hypertonic NaCl 573 cally in various animal species, including cats (Folkow et al, 1959(Folkow et al, , 1964Hilton and Spyer, 1971;Iijima and Philippu, 1980;Philippu and Schartner, 1976), rabbits (Gellman et al, 1981), and rats (Faiers et al, 1976;Kristt, 1975). Folkow et al (1959) were the first to identify the anterior hypothalamus in cats as a circumscribed brain area from which depressor responses can be elicited consistently by electrical stimulation.…”

Section: Discussionmentioning

confidence: 99%

Chronic cerebroventricular infusion of hypertonic sodium chloride in rats reduces hypothalamic sympatho-inhibition and elevates blood pressure.

Miyajima¹,

Buñag²

1984

Circulation Research

View full text Add to dashboard Cite

SUMMARY. To determine whether or not salt loading restricted to the brain would elevate blood pressure, chronically implanted osmotic minipumps were used to infuse hypertonic sodium chloride solutions made in artificial cerebrospinal fluid into a jugular vein intravenously or the third cerebral ventricle, intracerebroventricularly, for 11 days in awake rats. During intracerebroventricular infusion of hypertonic sodium chloride, tail-cuff systolic pressures began to rise on day 4 and were significantly elevated by day 9. In contrast, infusions of either artificial cerebrospinal fluid alone, intracerebroventricularly, or hypertonic sodium chloride, intravenously, were ineffective. Confirming the blood pressure elevation thereby detected, systolic and mean pressures recorded directly from indwelling aortic catheters after the same rats had been anesthetized with urethane on day 11, were also significantly higher following intracerebroventricular infusion of hypertonic sodium chloride than after infusion of artificial cerebrospinal fluid alone. Magnitude of depressor and sympatho-inhibitory responses elicited by graded electrical stimulation of the anterior hypothalamus invariably increased with the current strength used for stimulation. At all current strengths used for hypothalmic stimulation, depressor responses as well as attendant decreases in sympathetic neural firing, were smaller in rats that had been infused intracerebroventricularly with hypertonic sodium chloride than in any of the controls. Inhibition seemed specific for the anterior hypothalamus because pressor responses to stimulation of the ventromedial hypothalamus were the same whether or not the intracerebroventricular infusion contained hypertonic sodium chloride. An explanation based on diminished cardiovascular sensitivity also appeared unlikely, since depressor responses to intravenously injected histamine were almost equal in both groups. Our results are compatible with the interpretation that hypertonic sodium chloride infused chronically into the 3rd ventricle acts by reducing anterior hypothalamic inhibition of sympathetic vasomotor tone, and that this, in turn, then elevates blood pressure. (Circ Res 54:566-575, 1984) ALTHOUGH the hypertensive effects of excessive salt intake in rats have often been attributed to peripheral sympathetic or renal pressor mechanisms, recent evidence suggests that a centrally induced sympathetic overactivity may also be involved. Together with the blood pressure elevation produced by deoxycorticosterone acetate (DOCA)-salt pretreatment, norepinephrine turnover decreases in the hypothalamus and brainstem (Nakamura et al., 1971; van Ameringen et al., 1977). In Dahl salt-sensitive rats, dietary salt loading enhances pressor responsiveness to intracerebroventricular (icv) injections of hypertonic saline solution (Ikeda et al., 1978) and to electrical stimulation of the ventromedial hypothalamus (Bunag et al., 1983). Furthermore, the resulting hypertension is greatly attenuated after either chemical destructio...

show abstract

Section: Discussionmentioning

confidence: 99%

Chronic cerebroventricular infusion of hypertonic sodium chloride in rats reduces hypothalamic sympatho-inhibition and elevates blood pressure.

Miyajima¹,

Buñag²

1984

Circulation Research

View full text Add to dashboard Cite

show abstract

“…Although there is substantial evidence to indicate exaggerated spinal autonomic reflexes it seems likely that the absence of inhibitory supra-spinal influences is important. There is also evidence suggesting the exis tence of vasodilatory pathways (Folkow & Rubenstein, 1965;Kristt, 1975;Reis et at., 1975), the absence of which may be yet another contributing factor. Studies using infusions of noradrenaline (Mathias et at., 1976b) lend some support to these observations.…”

mentioning

confidence: 99%

Cardiovascular aspects of autonomic dysreflexia since Guttmann and Whitteridge (1947)

Frankel

Mathias

1979

Spinal Cord

View full text Add to dashboard Cite

word: Dysreflexia.'AUTONOMIC DYSREFLEXIA ' in patients with high spinal cord lesions has been used in reference to the changes induced by a variety of stimuli which occur in target organs supplied by the sympathetic and parasympathetic nervous systems. The earliest description of the symptoms of autonomic dysreflexia which we have been able to find is by Hilton (1860) who described a 21-year-old man with a tetraplegia complete below C5 segment whose 'bowels (did) not open without medicine (senna). On some days he has peculiar sensations of chilliness, becoming pale, then feels hot and flushed both at defaecation and micturition. The more constipated the bowel, the more these peculiar sensations are experienced.' Hilton described these phenomena but drew no conclusion.It was during World War I that Head and Riddoch made detailed observations of autonomic dysreflexia in patients with spinal cord injuries. They accurately described the responses of sweat glands, genitalia, urinary bladder and rectum which were evoked by cutaneous stimulation below the level of the lesion and by injection of fluid into the bladder and the bowel (Head & Riddoch, 1917;Riddoch, 1917). Riddoch (1917) also described the initial stage of spinal shock during which tendon reflexes could not be elicited and retention of urine and faeces occurred. This stage was followed by the second stage of reflex activity when stimulation of the skin produced sweating around and above the segmental level of the lesion, evacuation of the bladder and rectum and erection of the penis and seminal emission important components of the 'mass reflex'.In recently injured patients with high spinal cord injuries who are in spinal shock there is minimal cardiovascular reflex activity presumably because both the parasympathetic and sympathetic pathways in the isolated spinal cord are depressed (Mathias et al., , 1979a. Pronounced cardiovascular changes, however, occur when spinal cord reflex activity returns. These were classically described by Guttmann and Whitteridge (1947) in patients with lesions at or above the level of T 5 during distension of the urinary bladder. They reported marked hypertension, a decrease in pulse rate, change of rhythm on the electrocardiograph (in particular extrasystoles), vasodilatation of the face, neck and nasal mucosa and vasoconstric tion of fingers and toes. The patients complained of flushing and sweating of the face and neck, blockage of nasal air passages and headache. The authors thought these were important alarm symptoms of visceral activity in parts of the paralysed body. Since then there have been numerous reports which have confirmed Gutt mann and Whitteridge's pioneering observations on the cardiovascular changes occurring during autonomic dysreflexia in patients with high thoracic and cervical spinal cord lesions. Similar changes also occur during cutaneous stimulation 46

show abstract

Changes in the microcirculation in the rat mesentery and skeletal muscles correlating with the systemic arterial pressure during hypothalamic stimulation

Veit¹,

Chernukh

1980

Bull Exp Biol Med

View full text Add to dashboard Cite

Diencephalic vasodepressor responses independent of heart rate changes

Cited by 7 publications

References 10 publications

Chronic cerebroventricular infusion of hypertonic sodium chloride in rats reduces hypothalamic sympatho-inhibition and elevates blood pressure.

Chronic cerebroventricular infusion of hypertonic sodium chloride in rats reduces hypothalamic sympatho-inhibition and elevates blood pressure.

Cardiovascular aspects of autonomic dysreflexia since Guttmann and Whitteridge (1947)

Changes in the microcirculation in the rat mesentery and skeletal muscles correlating with the systemic arterial pressure during hypothalamic stimulation

Contact Info

Product

Resources

About