Pathogenesis of Experimental Hypertension Produced by Carotid Sinus Area Constriction in Dogs

Crandall, Earle E.; Mccrorey, H. L.; Sukowski, E. J.; Wakerlin, G. E.; Graham, Lori; Keith, Bowering; Speer, R. J.

doi:10.1161/01.res.5.6.683

Cited by 17 publications

(6 citation statements)

References 9 publications

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“…It should be noted in both Crandall et al (17) and Burstyn et al (12) studies, the manipulation affected only the carotid baroreceptors, and aortic baroreceptors should have been functioning normally. Because denervation of carotid baroreceptors alone does not lead to changes in MAP (33,45,56), presumably because aortic baroreceptors provide sufficient input to inhibit increased SNA, the question arises as to why MAP increases if afferent signals from carotid baroreceptors are simply reduced, as opposed to being eliminated.…”

Section: Baroreceptors and Vascular Compliancementioning

confidence: 94%

“…A principal criticism of the early reports that SAD caused hypertension is based on the observation that the stress associated with measuring the MAP by puncture caused the hypertension rather than denervation of the baroreceptors themselves (15). The same criticism does not apply to the data of Crandall et al (17) because even if there were some damage to the sinus nerves, the aortic baroreceptors should have remained functional. They also studied a group of SAD dogs and reported control pressures of 117 Ϯ 7 mmHg before and 189 Ϯ 16 mmHg after SAD.…”

Section: Baroreceptors and Vascular Compliancementioning

confidence: 99%

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Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure

Thrasher¹

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Thrasher, Terry N. Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure. Am J Physiol Regul Integr Comp Physiol 288: R819 -R827, 2005; doi:10.1152/ajpregu.00813.2004.-Whether arterial baroreceptors play a role in setting the long-term level of mean arterial pressure (MAP) has been debated for more than 75 years. Because baroreceptor input is reciprocally related to efferent sympathetic nerve activity (SNA), it is obvious that baroreceptor unloading would cause an increase in MAP. Experimental proof of concept is evident acutely after baroreceptor denervation. Chronically, however, baroreceptor denervation is associated with highly variable changes in MAP but not sustained hypertension. The ability of baroreceptors to buffer imposed increases in MAP appears limited by a process termed "resetting," in which the threshold to fire shifts in the direction of the pressure change and if the pressure elevation is maintained, it leads to a rightward shift in the relationship between baroreceptor firing and MAP. The most common hypothesis linking baroreceptors to changes in MAP proposes that reduced vascular distensibility in baroreceptive areas would cause reduced firing at the same pulsatile pressure and, thus, reflexively increase SNA. This review focuses on effects of baroreceptor denervation in the regulation of MAP in human subjects compared with animal studies; the relationship between vascular compliance, MAP, and baroreceptor resetting; and, finally, the effect of chronic baroreceptor unloading on the regulation of MAP.hypertension; sympathetic nerve activity THE SUSPICION THAT INCREASED sympathetic nerve activity (SNA) could play a role in the development of essential (i.e., primary) hypertension has been considered for a long time (24, 29, 37); however, definitive evidence that this suspicion is true has appeared only relatively recently. Increases in cardiac and renal norepinephrine spillover (an index of SNA to these organs) have been demonstrated in patients with borderline and mild essential hypertension (23). Moreover, direct measurements of muscle SNA via microneurography have indicated increased activity in subjects with essential hypertension (4, 67). The fact that increased SNA is detectable before established hypertension provides a known mechanism in the etiology of the condition; however, the cause of the increase in SNA is not known.It is generally agreed that essential hypertension arises from a combination of genetic and environmental influences (24). Thus the range of factors that could drive an increase in SNA is enormous. One of the best known and intensely studied of these factors is the reciprocal relationship between arterial baroreceptor input and sympathetic outflow. Experiments in the early part of the 20th century observed that denervation of baroreceptors in the carotid sinus and aortic arch (SAD) in experimental animals produced striking and highly variable increases in mean arterial pressure (MAP, see Ref. 29 for review of the early literature). However,...

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Section: Baroreceptors and Vascular Compliancementioning

confidence: 94%

Section: Baroreceptors and Vascular Compliancementioning

confidence: 99%

Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure

Thrasher¹

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…1 Their studies suggest that the persistent hypertension which follows may be initiated either by altered carotid sinus function or by a change in cerebral hemodynamics. 1 ' 2 The pathogenesis of this type of chronic hypertension is unknown and the possibility exists that it may be due to some altered humoral mechanism. Studies of others indicate that hypophysectomy in normotensive dogs does not necessarily lead to a fall in mean arterial pressure 3 ' 4 and in the dog, hypophysectomy does not prevent development of a modest renal hypertension following renal artery constriction.…”

mentioning

confidence: 99%

Antihypertensive Effect of Hypophysectomy in Dogs with Hypertension Following Bilateral Carotid Sinus Constriction

Hawthorne

Gaspar

1959

Circulation Research

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A chronic type of experimental hypertension has been produced in dogs by bilateral sinus area constriction. Hypophysectomy has a prolonged antihypertensive effect in dogs with persistent hypertension resulting from carotid sinus area constriction, while no decrease in mean arterial pressure is seen after hypophysectomy in normotensive control dogs. These findings suggest the possibility that altered hypophyseal function participates in the pathogenesis of this typ^ of hypertension.T HE experimental production of chronic hypertension in dogs by bilateral carotid sinus constriction has been reported by Wakerlin, Crandall, Frank, Johnson, Pom per, and Schmid.1 Their studies suggest that the persistent hypertension which follows may be initiated either by altered carotid sinus function or by a change in cerebral hemodynamics.1 ' 2 The pathogenesis of this type of chronic hypertension is unknown and the possibility exists that it may be due to some altered humoral mechanism. Studies of others indicate that hypophysectomy in normotensive dogs does not necessarily lead to a fall in mean arterial pressure 3 ' 4 and in the dog, hypophysectomy does not prevent development of a modest renal hypertension following renal artery constriction.5 It was our view that in dogs hypertensive after carotid sinus constriction, the finding of a consistent and chronic antihypertensive effect of hypophysectomy would suggest a pathogenic role for altered hypophyseal function. METHODSMongrel dogs of both sexes, generally weighing less than 12 Kg., were caged and fed the same standard diet. Each dog was allowed a period of one or more months of normotension, followed by bilateral carotid sinus constriction and a postoperative period of 3 or more months to allow for stabilization of the resulting hypertension. The bilateral carotid sinuses were constricted as described by Wakerlin 1 using the plastic clamps described 1 -2 and generously supplied to us by Dr. Wakerlin.After these dogs became hypertensive, they were hypophyseetomized and observed for periods of varying lengths. Nbrmotensive dogs, without prior carotid sinus constriction, were also hypophysectomized to observe the effect of complete hypophysectomy on their mean arterial pressure.Preoperatively the dogs were given 25 mg. of cortisone intramuscularly. Brain shrinkage was obtained by administering intravenously 50 ml. of 30 per cent glucose solution approximately 20 to 30 min. prior to surgery. Hypophysectomy was accomplished via a left transtemporal approach, following (in part) the principles of Gushing'. 0 The surgical technie was modified in that the entire pituitary was removed under direct vision by suction rather than with Gushing forceps.Glucose solution (30 per cent) was intravenously injected postoperatively to relieve increased intracranial pressure during the 24 hours immediately following surgery. Small maintenance doses of either prednisolone or cortisone (usually 12 mg. every third day, intramuscularly) were given. Postoperative therapy included antibiotics. Dogs in...

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“…It seems likely, therefore, that in the experiments of Crandall and co-workers the inadvertent disruption of the carotid sinus nerves and possibly damage to other buffer nerves could have been responsible for hypertension. 5 Koch also found in an occasional dog that moderate hypertension developed following disruption of the carotid sinus nerves alone." However, he observed the dogs for only a relatively short time.…”

Section: Discussionmentioning

confidence: 97%

Chronic Constriction of the External and Internal Carotid Arteries in Dogs: Its Effect on the Blood Pressure

Kezdi

1960

Circulation Research

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Narrowing of the internal and external carotid arteries by a clamp does not lead to hypertension if the carotid sinus nerves remain intact. Subsequent disruption of the carotid sinus nerves results in hypertension. It is concluded that the cause of the chronic hypertension in dogs with constriction of the carotid sinus is not due to altered cerebral hemodynamics, but rather to disruption of the carotid sinus nerves.

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Pathogenesis of Experimental Hypertension Produced by Carotid Sinus Area Constriction in Dogs

Cited by 17 publications

References 9 publications

Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure

Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure

Antihypertensive Effect of Hypophysectomy in Dogs with Hypertension Following Bilateral Carotid Sinus Constriction

Chronic Constriction of the External and Internal Carotid Arteries in Dogs: Its Effect on the Blood Pressure

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