Analysis of Design and Reactivity of Series‐coupled Vascular Sections in Spontaneously Hypertensive Rats (SHR)

Folkow, Björn; Hallbäck, Margareta; Lundgren, Yen; Weiss, Lilian; Albrecht, I.; Julius, Stevo

doi:10.1111/j.1748-1716.1974.tb05632.x

Cited by 55 publications

(49 citation statements)

References 2 publications

(2 reference statements)

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“…42 However, drastic and rapid pressure reductions may then more easily cause relative ischemia in brain and myocardium, because the amplifier properties and the raised R,^ will then cause more profound flow reductions. Otherwise, it is when precapillary structural adaptation encompasses all systematic circuits, as in hypertension, that it has deleterious long-term consequences, mainly because it then invites to the positive feedback interactions discussed earlier.…”

Section: Site Of Adaptation and Nature Of Stimulusmentioning

confidence: 99%

“…It is, however, likely that the pressure-induced changes in wall stress, together with the flow-dependent changes in chemical environment, activate appropriate local growth-modulating factors that, in the final analysis, direct the complex changes of vascular design. 2829 This local remodeling of the precapillary resistance vessels provides the basis for a long-term autoregulation of blood flow and of capillary pressure ("structural autoregulation" 42 as a correlate to short-term functional autoregulation). Thus, both are locally induced and both tend to keep flow and, far more importantly, capillary pressure constant during changes in MAP.…”

Section: Site Of Adaptation and Nature Of Stimulusmentioning

confidence: 99%

“…40 - 42 Assuming muscle strength per unit area to be essentially equal in, for instance, SHR. and WKY rats, the difference in media thickness is then reflected by the difference in maximal pressor response, as corrected for the prevailing difference in T b which can be deduced from the prevailing resistance values.…”

Section: Experimental Analysis In Ratsmentioning

confidence: 99%

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"Structural factor" in primary and secondary hypertension.

1990

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The history of research on the "structural factor" in primary hypertension is briefly reviewed, and the gradual realization of its important influence on the hemodynamics of hypertension is outlined, as seen from a "personal angle." Experiences from previous studies of normal vascular function in animals were decisive for our first hemodynamic demonstration concerning the "structural upward resetting" of the systemic resistance vessels in human primary hypertension. Subsequent quantitative studies in rats with primary and secondary hypertension complemented these studies, confirming that the critical structural changes are a rapid increase in precapillary resistance at full dilatation associated with an increase in wall/lumen ratio due mainly to media hypertrophy and occurring in both primary and renal hypertension. Analyses were also performed concerning cardiac, barostat, and venous structural resettings, which are briefly mentioned. In our first studies of human primary hypertension, we suggested that the structural factor might itself be genetically reinforced, and increasing evidence in favor of this view is now accumulating. It is further discussed how antihypertensive therapy should be directed primarily against the structural upward resetting, as dependent on the local pressure and "trophic" influences, and some of our results in rat models are outlined. Finally, as the structural factor at the systemic resistance level also invites positive feedback interactions with functional "pressor" influences, it is, in a way, more difficult to explain why 85-90% of people remain normotensive than how hypertension gradually develops in 10-15% of people. This points to some powerful and durable negative feedbacks, which are still poorly understood, because most so far known barostats are readily reset upward in hypertension. It is here that the Muirhead renomedullary depressor system, and perhaps also the unmyelinated baroreceptor-volume receptor afferents, may be of particular importance. {Hypertension 1990;16:89-101) D uring recent decades, the multifactorial nature of primary essential hypertension has become widely recognized; there are at least three major components that can be discerned.1 -2 Thus, in both humans and animals a porygenetic predisposition (the first component), random in humans but fairly uniform in each of the various rat strains, constitutes the sine qua non element behind the rise in blood pressure. The second component is environmental mechanisms, which interact with these various genetic makeups and are mainly composed of neurohormonal psychosocial influences and dietary factors such as salt intake. 1 -4 Then where does the third component, the "structural factor," fit in and how was its important role in hypertension discovered? As is the case in largely all tissues, structural cardiovascular adaptation is a normal and essentially local response to sustained aver-

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Section: Site Of Adaptation and Nature Of Stimulusmentioning

confidence: 99%

Section: Site Of Adaptation and Nature Of Stimulusmentioning

confidence: 99%

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"Structural factor" in primary and secondary hypertension.

1990

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“…It has been demonstrated that the number of patent precapillary arterioles is actually decreased in skeletal muscle of SHR. 28 Therefore, one might expect the number of patent postcapillary vessels to decrease to maintain tissue homeostasis. Hutchins * that R v is reduced in SHR hindparts and cremaster muscle, respectively.…”

mentioning

confidence: 99%

Pre- and postcapillary vascular responses to sympathetic nerve stimulation in DOCA-hypertensive dogs.

Brock¹,

Fleming²,

Diana³

1981

Hypertension

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SUMMARY Measurements of precapillary resistance (R.), postcapillary resistance (R v ), and mean capillary hydrostatic pressure (P c i) were made during sympathetic nerve stimulation (SNS) under constantflow perfusion in isolated hindlimbs from deoxycorticosterooe acetate (DOCA)-hypertensiTe dogs. We found that both pre-and postcapillary vascular responses to SNS were greater in the DOCA-hypertensive group when compared to the control group. Intraarterial injections of norepinephrine produced a dose-response curve for precapillary vessels in the hypertensive group that was asymmetrically shifted to the left (increased slope) and exhibited a significant decrease in vasoconstrictor threshold. These results, coupled with our earlier observations, suggest that the hyperresponslveness of the precapillary segment in DOCA-hypertensive dogs could be attributed to both structural and intrinsic alterations of the resistance vessels. We present evidence that suggests, however, that the increased postcapillary resistance with SNS may be explained by a structural alteration causing a decrease in the diameter of existing postcapillary vessels, or may be due to a decrease in the actual number of postcapillary vessels, or both. It is concluded that in this model of hypertension, postcapillary vascular changes also contribute to the overall increase in total peripheral resistance. The factors that contribute to this phenomenon remain unclear. In isolated hindlimbs from deoxycorticosterone acetate (DOCA)-hypertensive dogs, we previously demonstrated that the decreased venous distensibility was in part due to some form of structural alteration of the postcapillary segment. 10Hindlimbs from hypertensive dogs exhibited an increased venous resistance following maximal pharmacological vasodilation, as compared to control hindlimbs. The observed structural differences may be due to vascular hypertrophy, 11 an increase in vascular tissue water and electrolyte content ("waterlogging"), 13 ' » or both. There is additional evidence that the decreased venous distensibility in hypertension may also be due to increased venomotor tone. Takeshita and Mark* reported that venous distensibility increased significantly (20%) in patients with borderline hypertension following phentolamine infusion, but did not increase in normotensive patients. Likewise, Walsh et al.' found that hypertensive patients failed to demonstrate a decrease in venous distensibility after tilting, a phenomenon that occurred in normotensive patients. In experimental hypertension, venous responsiveness to norepinephrine 1 and adrenergic nerve stimulation" are enhanced.The present experiments were designed to study pre-and postcapillary vascular responses to sympathetic nerve stimulation (SNS) in deoxycorticosterone acetate (DOCA)-salt-induced hypertension. Our results demonstrate that the increased responses of the postcapillary vascular bed in the isolated hindlimbs from dogs with DOCA-salt hypertension may be due to one or more structural factors: 1) a decrease in the initi...

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“…Following local chemical sympathetic denervation with 6-hydroxydopamine, VSM in SHR hyperpolarized from a control value of -37 ± 0.6 to -51 ± 0.4 mV while E ra in WKY remained at -5 0 ± 0. N the spontaneously hypertensive rat (SHR), the elevated total peripheral resistance (TPR) accompanying development of hypertension has been attributed to: 1) structural adaptations in the arterial vessel wall 1 and the microvessel network, 2 and 2) increased vascular smooth muscle (VSM) tone. In turn, this elevated tone has been attributed to an elevated sympathetic neural input 1 4 and to alterations in the intrinsic mechanisms of the VSM membrane that regulate the concentration of cytosolic activator calcium (Ca).…”

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confidence: 99%

Response of venous membrane potentials to calcium blockade in spontaneous hypertension.

Stekiel¹,

Contney²,

Lombard³

et al. 1983

Hypertension

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SUMMARY In situ measurements of transmembrane potential (Em) were made in vascular smooth muscle cells (VSM) of small (250-500 /xm) veins in an externalized mesenteric loop in 13-to 15-weekold anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive controls (WKY). Following local chemical sympathetic denervation with 6-hydroxydopamine, VSM in SHR hyperpolarized from a control value of -37 ± 0.6 to -51 ± 0.4 mV while E ra in WKY remained at -5 0 ± 0.

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Analysis of Design and Reactivity of Series‐coupled Vascular Sections in Spontaneously Hypertensive Rats (SHR)

Cited by 55 publications

References 2 publications

"Structural factor" in primary and secondary hypertension.

"Structural factor" in primary and secondary hypertension.

Pre- and postcapillary vascular responses to sympathetic nerve stimulation in DOCA-hypertensive dogs.

Response of venous membrane potentials to calcium blockade in spontaneous hypertension.

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