Chronic hypothalamic stimulation in awake rats fails to induce hypertension.

Buñag, R D; Riley, E.J.

doi:10.1161/01.hyp.1.5.498

Cited by 19 publications

(3 citation statements)

References 19 publications

(12 reference statements)

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“…Behavioral and cardiovascular responses elicited upon subsequent electrical stimulation of the ventromedial hypothalamus were qualitatively similar to those described previously for the posterior 27 and anterior 20 hypothalamus. As current strengths used for stimulation were made stronger, behavioral effects also became progressively more pronounced, and four phases could be identified.…”

Section: Behavioral and Cardiovascular Effects Of Hypothalamic Stimulsupporting

confidence: 75%

Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness.

Buñag¹,

Tomita²,

Sasaki³

1982

Hypertension

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SUMMARY To determine whether diabetes predisposes rats to hypertension, tail-cuff systolic pressures were measured in male rats made diabetic by pretreatment with streptozotocin. From Weeks 2 through 7, diabetic rats weighed less but had higher systolic pressures than nondiabetic ones. Further comparisons made while the rats were anesthetized with urethane showed that pressor and sympathetic nerve responses to ventromedial hypothalamic stimulation, as well as pressor responses to injected vasopressin, were significantly reduced in the diabetic group. A generalized reduction of cardiovascular reactivity was considered unlikely because systemic pressor responses to norepinephrine and tyramine were unimpaired. Yet reflex bradycardia elicited by norepinephrine was enhanced indicating that baroreceptor resetting had not occurred. Thus, diabetic rats were characterized by hypertension, narrowed pulse pressure, bradycardia with increased reflex responses to norepinephrine, and reduced pressor responses to hypothalamic stimulation and to vasopressin. The successful induction of diabetes was confirmed not only by the presence of hyperglycemia, hypoinsulinemia, glycosuria, and abnormal glucose tolerance, but also by reductions in pancreatic weight, insulin, and /3-cell content. Although our results suggest that diabetic rats are predisposed to become hypertensive, other mechanisms such as hypothalamic depression may be activated to restrict further elevations in blood pressure. H YPERTENSION is generally believed to be more prevalent among diabetics than nondiabetics, 1 -2 but why this might be so is uncertain. Previous attempts to record blood pressure in rats with experimental diabetes have yielded equivocal results. Although blood pressure in normotensive rats is usually elevated by either alloxan 2 " 1 or streptozotocin, 5 -6 it has also been found unaffected 7 or even slightly decreased by streptozotocin. 8 In spontaneously hypertensive rats (SHR), blood pressure falls during the first few weeks after alloxan diabetes is induced, 4 6 9 but several months later becomes even higher than before. 3 From the Department of Pharmacology, College of Health Sciences and Hospital, University of Kansas Medical Center, Kansas City, Kansas.Supported by Research Grant AM 27660 from the National Institute of Arthritis, Metabolism, and Digestive Diseases.An abstract of this paper was published in Federation Proceedings 40: 391, 1981. Dr. Susumu Sasaku is a postdoctoral research fellow from the Second Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.Address for reprints: Dr. Ruben D. Bunag, Department of Pharmacology, University of Kansas Medical Center, 39th and Rainbow Boulevard, Kansas City, Kansas 66103.Received May 27, 1981; revision accepted December 7, 1981. While trying to characterize the cardiovascular changes occurring in normotensive rats that had been pretreated with streptozotocin, we found the ensuing diabetes accompanied by mild hypertension. Both blood pressure 10 and blood sugar" a...

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Section: Behavioral and Cardiovascular Effects Of Hypothalamic Stimulsupporting

confidence: 75%

Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness.

Buñag¹,

Tomita²,

Sasaki³

1982

Hypertension

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“…Increases in CBF-TR were noted in the PH, DMH, and VMH. Past work has shown that stimulation or disinhibition of the PH and DMH increases blood pressure, heart, and respiratory rate and escape-defense behavior (Bunag et al, 1975;Bunag and Riley, 1979;Shekhar et al, 1990;Samuels et al, 2004). With projections to midline thalamic nuclei and brainstem cardiovascular centers (Vertes et al, 1995;Vertes and Crane, 1996), the PH has been proposed to be in a position to receive converging sensory and limbic input and, thus, alter the levels of cerebral activation, as well as cardiovascular tone.…”

Section: Hypothalamusmentioning

confidence: 99%

Mapping cerebral blood flow changes during auditory-cued conditioned fear in the nontethered, nonrestrained rat

et al. 2006

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Conditioned fear (CF) is one of the most frequently used behavioral paradigms; however, little work has mapped changes in cerebral perfusion during CF in the rat-the species which has dominated CF research. Adult rats carrying an implanted minipump were exposed to a tone (controls, n = 8) or a tone conditioned in association with footshocks (CS group, n = 9). During reexposure to the tone 24 h later, animals were injected intravenously by remote activation with [14C]-iodoantipyrine using the pump. Significant group differences in regional CBF-related tissue radioactivity (CBF-TR) were determined by region-of-interest analysis of brain autoradiographs, as well as in the reconstructed, three-dimensional brain by statistical parametric mapping (SPM). CS animals demonstrated significantly greater, fear-enhanced increases in CBF-TR in auditory cortex than controls. The lateral amygdala was activated, whereas the basolateral/basomedial and central amygdala were deactivated. In the hippocampus and medial prefrontal cortex, CBF-TR increased significantly ventrally but not dorsally. Significant activations were noted in medial striatum and the thalamic midline and intralaminar nuclei. However, the ventrolateral/dorsolateral striatum and its afferents from motor and somatosensory cortex were deactivated, consistent with the behavioral immobility seen during CF. Significant activations were also noted in the lateral septum, periaqueductal gray, and deep mesencephalic nucleus/tegmental tract. Our results show that auditory stimuli endowed with aversive properties through conditioning result in significant redistribution of cerebral perfusion. SPM is a useful tool in the brain mapping of complex rodent behaviors, in particular the changes in activation patterns in limbic, thalamic, motor, and cortical circuits during CF.

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“…ously described, 13 current thresholds were determined in each rat by starting stimulation with 50 fiA and progressively increasing current strength by 20 fiA increments until a 2 mm Hg increase in mean pressure occurred.…”

Section: Group 1 Terminal Experiments: Effects Of Bilateral Electrolymentioning

confidence: 99%

Aging escalates baroreceptor reflex suppression by the posterior hypothalamus in rats.

Tanabe

Buñag

1991

Hypertension

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To examine whether baroreceptor reflex regulation by the posterior hypothalamus becomes modified with age, we compared baroreceptor reflex sensitivity and hypothalamic responsiveness in 2- and 10-month-old rats anesthetized with urethane-chloralose. Hypothalamic regulation of baroreceptor reflex sensitivity was assessed by recording responses to intravenously infused phenylephrine and afferent aortic nerve stimulation after sham operation or electrolytic destruction of the posterior hypothalamus. Regardless of age, reflex bradycardia and sympathoinhibition elicited during pressor responses to phenylephrine, as well as all cardiovascular and sympathetic nerve responses to afferent aortic nerve stimulation, were stronger in rats with bilateral hypothalamic lesions than in age-matched, sham-operated controls. Distinctively, because baroreceptor reflex sensitivity differed with age only in sham-operated controls but not in lesioned rats, we concluded that age-related differences in baroreceptor reflex sensitivity had been abolished by posterior hypothalamic lesions. Other experiments were then performed to compare responses to graded electrical stimulation of the posterior hypothalamus in baroreceptor-intact rats. Pressor and sympathoexcitatory responses to hypothalamic stimulation were larger, and stimulus thresholds were lower at 10 than at 2 months of age thereby suggesting that hypothalamic responsiveness had increased with age. Our results are in accord with the interpretation that aging exacerbates the baroreceptor reflex suppression normally exerted by the posterior hypothalamus.

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Chronic hypothalamic stimulation in awake rats fails to induce hypertension.

Cited by 19 publications

References 19 publications

Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness.

Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness.

Mapping cerebral blood flow changes during auditory-cued conditioned fear in the nontethered, nonrestrained rat

Aging escalates baroreceptor reflex suppression by the posterior hypothalamus in rats.

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