Sustained pressore responsiveness to prolonged hypothalamic stimulation in awake rats

Buñag, R D; Riley, E.J.; Montello, Michael

doi:10.1152/ajplegacy.1976.231.6.1708

Cited by 18 publications

(9 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present findings cannot be artifacts caused by anesthesia because enhanced hypothalamic pressor responsiveness has been observed repeatedly even in awake or unanesthetized spontaneously hypertensive rats (3,27). In normotensive rats, pressor responses to hypothalamic stimulation are slightly increased by urethane anesthesia but unaffected by positive-pressure respiration or drug-induced neuromuscular blockade (28); an appreciable effect of these experimental conditions on the results described here is, therefore, unlikely.…”

Section: Resultsmentioning

confidence: 45%

“…Various stresses (noise, restraint, light, or vibration) increase blood pressure more in spontaneously hypertensive than in normotensive rats (20,30) but whether the elevation eventually persists is unknown. With repeated hypothalamic stimulation pressor responses remain enhanced in awake spontaneously hypertensive rats, but basal pressure levels are unchanged even after several hours (27). More prolonged hypothalamic stimulation like that which has been used to elevate systolic pressure progressively in normotensive rats (31) could conceivably exacerbate development or maintenance of spontaneous hyper-, tension.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Sympathetic Hyperactivity during Hypothalamic Stimulation in Spontaneously Hypertensive Rats

Takeda¹,

Buñag²

1978

J. Clin. Invest.

109

View full text Add to dashboard Cite

A B S T R A C T To (2) found the vasodepressor effects produced by cutting neural connections between the hypothalamus and mesencephalon more pronounced in spontaneously hypertensive than in normotensive rats. Second, Buniag et al. (3) later showed that pressor responses elicited by electrical stimulation of the posterior hypothalamus were larger in awake rats with spontaneous hypertension than in normotensives or in those with deoxycorticosterone acetate-salt (Doca)l hypertension. How these differences are caused is uncertain. It is well known that hypothalamic activation augments sympathetic discharge (4-6) and if hypothalamic hyperactivity is partly responsible for spontaneous hypertension then hypothalamic stimulation could increase sympathetic vasomotor discharge more in spontaneously hypertensive than in other rats. To test this assumption we compared spike potentials recorded from sympathetic nerves in spontaneously hypertensive rats during electrical stimulation of the

show abstract

Section: Resultsmentioning

confidence: 45%

Section: Resultsmentioning

confidence: 99%

Sympathetic Hyperactivity during Hypothalamic Stimulation in Spontaneously Hypertensive Rats

Takeda¹,

Buñag²

1978

J. Clin. Invest.

109

View full text Add to dashboard Cite

show abstract

“…7 , 1 7 and fixed to the skull with stainlesssteel screws and dental cement. 18 For recording blood pressure, an indwelling catheter was inserted into the right femoral artery with its outer end passed subcutaneously to emerge at the nape of the neck. One day later, each rat was kept in a round open-topped cage, awake but partly restrained by a harness-and-swivel arrangement; 19 a harness wrapped around the rat's chest was attached by a steel spring to a slip-ring swivel (Airflyte Electronics, Bayonne, New Jersey) placed above the cage.…”

Section: Direct Recording Of Responses To Hypothalamic Stimulation Inmentioning

confidence: 99%

Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness.

Buñag¹,

Tomita²,

Sasaki³

1982

Hypertension

View full text Add to dashboard Cite

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...

show abstract

“…Four phases of progressively intensified behavior, resembling that described before for the posterior hypothalamus, 10 '…”

Section: Pressor Responsiveness In Awake Rats Previously Exposed To Smentioning

confidence: 57%

“…During the first operation (done the day after the last shaking session), concentric electrodes (NE-100, custom made with chronic connectors by Rhodes Medical Instruments, Woodland Hills, CA) inserted in the anterior hypothalamus at stereotaxic coordinates anteroposterior 6.0, lateral 1.2, and dorsoventral -2.5, were fixed with dental cement to stainless steel screws embedded in the skull. 10 Two days later, a second operation was performed to insert an indwelling cannula into the lower abdominal aorta via a common iliac artery; the outer end of the cannula was passed subcutaneously to emerge at the nape of the neck. 11 Acute experiments were done the next day after aortic cannulation, or 4 days after the last exposure to daily shaker stress.…”

Section: Surgical Preparation For Acute Studiesmentioning

confidence: 99%

Spontaneous remission of hypertension in awake rats chronically exposed to shaker stress.

Buñag¹,

Takeda²,

Riley³

1980

Hypertension

Self Cite

View full text Add to dashboard Cite

SUMMARY Hypertension was induced experimentally by subjecting rats to vigorous shaking, 4 hours (at random) daily for 14 weeks. Systolic pressures measured with the tail-cuff method began to rise after the first week and were significantly derated on Weeks 3, 4, 6, 7, and 8, but reverted to normotensive levels thereafter despite continued shaking. A similar hypertension was then induced in another group of rats and when spontaneous remission occurred, pressor responsiveness was tested on the eleventh week by recording aortic pressures from indwelling catheters. Pressor responses to further shaking or electrical stimulation of the anterior hypothalamus were smaller in shaker-stressed than in control rats, while those to injected norepinephrlne were almost the same in both groups. Spike potentials recorded from postganglionlc sympathetic (splanchnic) nerves showed higher baselines but smaller increases in neural firing during hypothalamic stimulation in shaker-stressed than in control rats. These results suggest that while shaker stress alone can induce hypertension, the resulting blood pressure elevation is not sustained, perhaps because adaptation within the central nervous system concurrently reduces pressor responsiveness. action to stress, and based on the assumption that with frequent repetition the pressure elevation eventually becomes sustained, chronic exposure to stress has often been used for inducing experimental hypertension. Air blasts, 1 intermittent decompression, 2 aversive operant conditioning,' psychosocial stimuli, 4 and a mixture of shaking, noise, and flashing lights," have all been found effective in making rats hypertensive. Because the hypertension thus induced can be prevented by chemical sympathectomy with 6-hydroxydopaminc" or by doses of amethyl tyrosine that deplete brain catecholamines selectively, 7 the involvement of central sympathetic mechanisms has been proposed. Chronic exposure to noise and flashing lights requires a precisely controlled laboratory environment that is more elaborate and expensive to set up than one based on shaking alone. Whether shaking (henceforth referred to as shaker 311 stress), which is more potent than either noise or flashing light in eliciting pressor or tachycardiac effects," can induce hypertension when applied alone is unknown. While attempting to resolve this question, we found the resulting blood pressure elevation unsustained. Consequently, additional experiments were done to determine whether pressor and neural responses to hypothalamic stimulation had been altered by previous exposure to shaker stress.Methods Two groups of 7-week-old female rats of the Sprague-Dawley strain, were purchased from Hilltop Laboratory Animals, Inc. (Chatsworth, CA) and randomly divided into control and experimental subgroups. Of 18 rats in the first group, half were used as controls and the others exposed to shaker stress manipulation for 14 weeks while systolic pressures, heart rates, and body weights were measured once weekly. A second group of 24 rats (12 contro...

show abstract

Sustained pressore responsiveness to prolonged hypothalamic stimulation in awake rats

Cited by 18 publications

References 0 publications

Sympathetic Hyperactivity during Hypothalamic Stimulation in Spontaneously Hypertensive Rats

Sympathetic Hyperactivity during Hypothalamic Stimulation in Spontaneously Hypertensive Rats

Streptozotocin diabetic rats are hypertensive despite reduced hypothalamic responsiveness.

Spontaneous remission of hypertension in awake rats chronically exposed to shaker stress.

Contact Info

Product

Resources

About