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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility of changes in the adrenergic innervation of blood vessels in experimental hypertension was investigated by measuring arterial norepinephrine content, neuronal uptake of norepinephrine, and the neurogenic contractile response in rabbits made hypertensive by partial constriction of the abdominal aorta proximal to the kidneys. Two to 3 weeks after surgery, norepinephrine content was increased in the arteries above the ligature, where arterial blood pressure was increased, but not in the arteries below the ligature, where arterial blood pressure was normal, in the heart, or in the veins. Neuronal norepinephrine uptake per unit length of vessel and the neurogenic contractile response increased with the rise in arterial blood pressure. The neurogenic contractile response can be taken as an indication of an increase in transmitter release. The results taken together suggest an increase in the function and possibly the amount of the adrenergic neuroneal terminal in hypertension. Since the distributions of the changes in the adrenergic innervation and the increases in smooth muscle cell proliferation in hypertension are similar, these two processes may be interrelated.
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PMID:Evidence for an increase in adrenergic nerve function in blood vessels from experimental hypertensive rabbits. 24 8

Asphyxia can cause neurologic damage in the fetus, but there are few data relating severity or duration of asphyxia to the degree of cerebral damage. We report cerebral histologic and electrophysiologic changes after asphyxia in chronically instrumented late-gestation fetal sheep. We reduced uterine blood flow to produce an ascending aortic blood oxygen content less than 1.5 mM for either 30 or 60 min (n = 13). In a subsequent protocol (n = 6), if full occlusion of the common uterine artery for 15 min did not reduce the EEG voltage to less than 20% of baseline, supplementary maternal hypoxia was added for a maximum of 120 min. Histologic outcome was assessed 3 d postinsult. Uterine artery occlusion resulted in severe hypoxemia, hypercarbia, acidosis, and an initial hypertension and bradycardia. Eight of 14 surviving fetuses showed neuronal damage, with greatest loss in the parasagittal cortex, striatum, and the CA1/2 region of the hippocampus. Neuronal damage was strongly associated with the percentage of decrease in blood pressure during the insult (r = 0.75, p less than 0.005) but not with the degree of hypoxia. No other factor was independently predictive, but, when considered separately, pH (r = 0.54; p less than 0.05) and loss of intensity of the EEG (r = 0.61, p less than 0.02) at the end of asphyxia were also correlated with outcome. The pH fell to less than 7.0 in six of eight fetuses with damage, whereas it remained greater than 7.0 in five of six without damage (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral histologic and electrocorticographic changes after asphyxia in fetal sheep. 160 25

In order to elucidate the pathophysiology involved in Powers' intermittent vertebral artery compression syndrome, the author investigated sympathetic and parasympathetic changes produced by stimulation of nerves around the proximal vertebral artery (the vertebral nerve) in anesthetized and immobilized cats. These changes were observed mainly through pupillary changes, pulse and blood pressure, evoked potentials in the lateral horn of the upper thoracic cord (centrum ciliospinale), in the cervical sympathetic trunk, and in the short ciliary nerve. Electrical stimulation of vertebral nerve and local application of K ion around the vertebral artery produced stimulus-dependent ipsilateral mydriasis; when stimulation of higher strength was applied pronounced ipsilateral and mild contralateral mydriasis and hypertension occurred. Electrical stimulation of perivascular tissue around the subclavian artery proximal to origin of the vertebral artery showed ipsilateral mydriasis; while on stimulating the distal subclavian, the costcervical, the omocervical and the internal thoracic arteries did not show any pupillary response. Neuronal discharges in the lateral horn of upper thoracic cord and in the cervical sympathetic trunk showed stimulus-dependent increases on stimulating the vertebral nerve; while, inhibitory responses were observed in the short ciliary nerve formed by parasympathetic nerve fibers. From the data available, it seems likely that the stimulation of periarterial neural structure of the vertebral artery produced sympathetic excitatory as well as parasympathetic inhibitory neuronal discharges simultaneously may probably be derived from the integrating autonomic center in the hypothalamus.
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PMID:[Effects of stimulation of the vertebral nerve around the proximal vertebral artery on pupil and the autonomic nervous system--a contribution to pathophysiology of Powers' intermittent vertebral artery compression syndrome]. 163 32

Neuronal organisation of hypothalamo-bulbar mechanisms of regulation of vascular tonus was studied in anesthetised and immobilised cats. The descending influence of posterior, tuberal and anterior structures of the hypothalamus on the activity of antidromically identified sympatho-activating reticulospinal neurons of the ventrolateral region of medulla oblongata is realised by mono-, oligo- and polysynaptic mechanisms. Chronic neurogenic hypertension was induced in rats by overloading the higher nervous activity. Arterial hypertension did not develop in chemically desympathized cats. Central and peripheral neurohumoral mechanisms of vascular tonus regulation are discussed.
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PMID:[The physiological mechanisms of the neurohumoral regulation of vascular tonus]. 168 35

Neuronal and glial cultures from the hypothalamic-brain stem areas of 1-day-old normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rat brains stained positively with atrial natriuretic peptide (ANP)-specific antibodies. The endogenous levels of the ANP immunoreactivity in WKY neuronal and glial cultures were 17.0 +/- 2.2 and 14.3 +/- 2.7 pg/mg, respectively. Comparable neuronal and glial cultures from SH rat brains contained a 48 to 70% decrease in the endogenous ANP immunoreactivity levels. Culture media from both brain cell types also contained ANP immunoreactivity, the levels of which are significantly higher than those found in the cells. However, similar to endogenous levels, the media levels of immunoreactive ANP in SH neuronal and glial cultures were significantly reduced compared with WKY brain cultures. These observations demonstrate that endogenous ANP-like immunoreactivity is found in neuronal and glial cells and is released into the media. The levels of peptide are reduced in cultures of SH compared with WKY cultures, suggesting a genetically controlled difference between the hypertensive and normotensive rat strains long before hypertension develops.
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PMID:Immunoreactive atrial natriuretic peptide in neuronal and glial cells of spontaneously hypertensive rat brain. 213 92

Using in vitro hypothalamic brain slices, differences in angiotensin II (AII) sensitivity of neurons in the organum vasculosum lamina terminalis (OVLT) region were compared between spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY). AII, the AII competitive antagonist saralasin, and L-glutamate were micropressure-applied onto OVLT neurons. AII excitation of SHR neurons was blocked or antagonized by simultaneous application of saralasin, evoked at significantly lower thresholds and displayed exaggerated periods of postactivity compared to OVLT neurons in preparations taken from WKY controls. Neuronal responses to L-glutamate were similar between the two rat strains. Differences in neuronal sensitivity to AII may be causally linked to hypertension in SHR.
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PMID:Altered angiotensin II sensitivity of neurons in the organum vasculosum lamina terminalis region of the spontaneously hypertensive rat. 289 61

Angiotensin II (AII) sensitivity of neurons in the region of the organum vasculosum laminae terminalis (OVLT) was examined electrophysiologically using in vitro hypothalamic brain slices taken from 4-, 9- and 14-week-old spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Micropressure application of AII, its competitive antagonist saralasin, and L-glutamate revealed that neurons in this region of SHR were significantly more sensitive to AII than cells in age-matched WKY preparations. Neuronal sensitivity to L-glutamate was similar between SHR and WKY rats at all ages. Following electrophysiological study, hypothalamic and cortical brain slices were assayed for 125I-labelled AII binding. AII receptor binding in the hypothalamic slices from SHR was elevated significantly above binding in WKY hypothalamic slices at 4, 9, and 14 weeks of age. In contrast, AII binding in cortical slices taken from SHR and WKY rats was similar. These data suggest that altered neuronal AII-sensitivity is not a consequence of hypertension development in SHR and may contribute to its development.
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PMID:Development of angiotensin II-sensitive OVLT neurons in SHR and WKY rats. 289 65

The tissue content of norepinephrine, dopamine, and epinephrine was determined in different zones of the kidney in normotensive Sprague-Dawley and Otago Wistar rats and in genetically hypertensive Otago Wistar rats. One kidney in each animal was chronically denervated to allow estimation of the neuronal contribution to renal catecholamine content. In all strains, the renal cortex contained negligible amounts of nonneuronal norepinephrine and dopamine, while outer and inner medullary layers contained progressively larger amounts. Nonneuronal epinephrine was distributed fairly evenly through cortex and medulla. Neuronal norepinephrine content was similar in inner and outer cortex, substantially less in outer medulla, and not discernible in inner medulla. The amounts of neuronal dopamine were consistent with its localization predominantly in noradrenergic nerves. The renal cortices of normotensive Wistar rats contained more neuronal norepinephrine and less neuronal dopamine than those of Sprague-Dawley rats, and the cortices of hypertensive Wistar rats contained slightly more norepinephrine than those of normotensive Wistar rats. In both normotensive strains, long-term salt loading decreased selectively the neuronal norepinephrine in renal cortex. By contrast, in hypertensive animals, cortical norepinephrine was not reduced by salt loading. These results indicate that the genetically hypertensive rat may have an abnormal sympathetic reflex response to increased blood volume.
Hypertension 1986 Feb
PMID:Catecholamines in kidneys of normotensive and genetically hypertensive rats. Effects of salt load. 394 89

Changes in relative metabolic requirements and neuronal densities in the nucleus commissuralis (NC) and nucleus medialis (NM) of the nucleus tractus solitarius were studied in spontaneously hypertensive rats (SHR) during development. The changes in relative metabolic requirements in the two subnuclei of SHR between 2 and 12 weeks of age were similar to those previously reported for normotensive WKY at the same ages. However, the relative metabolic activity in the NC of 2- and 4-week SHR was significantly higher than in normotensive rats. The differences in metabolic requirements of the NC could not be explained by differences in the neuronal densities of this subnucleus in young SHR and may reflect abnormalities in developmental or functional activities in the pre-hypertensive rat. Neuronal densities in the NC of 8- and 12-week SHR and in the NM of 4-, 8- and 12-week SHR were significantly higher than in WKY controls. Differences in the neuronal densities in the NC and NM of SHR may be explained by a smaller brain size characteristic of this strain, but differences in the NC of SHR suggest that the alterations may underlie or result from the cardiovascular abnormalities associated with the spontaneous hypertension of this strain.
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PMID:The development of two subnuclei of the nucleus tractus solitarius in spontaneously hypertensive rats. 669 55

Neuronal nitric oxide synthase (nNOS) has been suggested to be involved in cardiovascular homeostasis. We studied the regulation of nNOS expression, determining nNOS mRNA expression levels in various tissues in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We also investigated the effects of antihypertensive treatment with the angiotensin II antagonist hydralazine or reserpine on nNOS mRNA expression. The expression levels of nNOS mRNA and nNOS protein were determined by Northern and Western blot analysis, respectively. NADPH-diaphorase histochemistry was used to identify cells in the adrenal medulla that expressed nNOS. No significant differences in expression levels in SHR and WKY were observed in the cerebellum and brain stem. nNOS mRNA expression levels in the decapsular portion of the adrenal gland were developmentally modulated and in a 24-week-old WKY were 2.5 times higher than in an age-matched SHR. This reduced expression of nNOS mRNA in the decapsular portion of the adrenal gland of SHR seemed to be a result of hypertension in the SHR, because administration of either an angiotensin II antagonist (TCV-116) or hydralazine upregulated nNOS mRNA expression in both SHR and WKY. Marked augmentation of nNOS mRNA expression in the decapsular portion of the adrenal gland by reserpine treatment suggested an intimate relation between nNOS in the decapsular portion of the adrenal gland and the sympathoadrenal system. Reserpine treatment also increased the expression of nNOS protein; however, reserpine treatment did not affect the distribution pattern of nNOS-positive cells (NADPH-diaphorase-positive cells) in the adrenal medulla.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Mar
PMID:Regulation of neuronal nitric oxide synthase in rat adrenal medulla. 753 41


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