The Present Status of the Autoregulation Theory of the Pathogenesis of Hypertension

Korner, Paul I.

doi:10.1111/j.1440-1681.1980.tb00103.x

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…This hemodynamic change, i. e. an increase in CO converts to an increase in TPR, was reported by Borst and Borst-de Geus (2) and Ledingham and Cohen (15), and explained by the autoregulation theory (2, 4, 10, 15), but this theory is under controversy (9,14). Our acute volume expansion produced three different hemodynamic responses.…”

Section: Discussionsupporting

confidence: 53%

“…The enhanced sympathetic activity and renin-angiotensin system may contribute to the early increase in TPR. The reports of an initial increase in TPR without a preceding increase in CO cast doubts on the autoregulation theory and Korner (14) stressed the importance of structural changes of heart and vessels. In this acute experiment we demonstrated that initial increase in CO was always observed before the increase in TPR.…”

Section: Discussionmentioning

confidence: 97%

“…The systemic auto-regulation theory (4, I0), participation of sympathetic nervous system (12,22), vasopressin (5,12), structural changes in heart and vessels (14) have been advocated to exp|ain this vasoconstriction. Recently, an ouabain-iike substance has received considerable attention because of its inhibitory action against Na+-K § in vascular smooth muscle cells (I,8,II).…”

Section: Introductionmentioning

confidence: 99%

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Effect of ouabain on hemodynamics in acute volume expanded hypertensive dogs

et al. 1989

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To evaluate possible roles of endogenous Na+-K+-ATPase inhibitors in vasoconstricted blood pressure elevation produced by acute volume expansion, we administered ouabain (Na+-K+-ATPase inhibitor) intravenously (30 micrograms/kg) for 10 min to dogs, 3 h after volume expansion with dextran in lactated Ringer's solution (20 ml/kg, for 1 h). Acute volume expansion resulted in the elevation of blood pressure associated with an increase in cardiac output. In some dogs the blood pressure remained elevated with gradual increase in total peripheral resistance (Group I) or with sustained high cardiac output (Group II), and in other dogs (Group III) it returned to the control level. Ouabain administration elevated the blood pressure and total peripheral resistance in these groups and sham dogs which did not have volume expansion. And these effects of ouabain were not correlated with the degree of blood pressure or vasoconstriction produced by volume expansion. Thus, it is not likely that endogenous Na+-K+-ATPase inhibitors increased to produce vasoconstricted hypertension after acute volume expansion.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Effect of ouabain on hemodynamics in acute volume expanded hypertensive dogs

et al. 1989

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“…The theory of systemic autoregulation as a summation of local autoregulation was proposed by Guyton et al 7 and Coleman et al 8 to explain the vasoconstriction after an initial increase in the CO. However, Korner 10 and other investigators 19 -21 found two hemodynamic patterns different from that found by Guyton et al: Volume expansion produced 1) vasoconstricted hypertension without a preceding increase in the CO and 2) cardiac output-dependent hypertension without subsequent increase in the TPR. The demonstration of these two patterns throws doubt on the theory of autoregulation.…”

Section: Discussionmentioning

confidence: 65%

Contribution of the baroreflex afferent nerves to the production of vasoconstricted hypertension in volume-expanded dogs.

Otsuka

Ogihara

Mikami

et al. 1989

Circulation Research

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Dextran in lactated Ringer's solution (20 ml/ kg) was infused for 1 hour into anesthetized dogs with slnoaortic denervation and vagotomy (deafferentatlon; n=10) and dogs treated with hexamethonium (de-efferentation; n = 13) to compare with our previous observation in dogs with an intact autonomic nervous system (control, n-34). During the infusion, increase in blood pressure associated with increase in cardiac output was observed in all three groups. The increases in blood pressure were larger in the two groups with an impaired autonomic nervous system. In the recovery period, the control dogs and the hexamethonium-treated dogs showed gradual increases in total peripheral resistance and in vasoconstricted hypertension 3 hours after stopping the infusion. In contrast, the dogs with sinoaortic denervation and vagotomy did not show any increase in total peripheral resistance. The vasoconstricted groups showed peaks of natriuresis soon after the infusion, not 3 hours after the infusion when vasoconstriction was observed, although the dogs with deafferentation did not show a significant increase in natriuresis. Norepinephrine (0.5 ftg/kg) was administered intravenously before and after volume expansion, and the pressor responses in the three groups after volume expansion were enhanced similarly (143%, 128%, and 136%, respectively). These results indicate that the afferent signals from peripheral vessels to the brain contribute to the production of vasoconstricted hypertension after acute volume expansion and that the vasoconstriction is independent of pressor hypersensitivity and is dissociated in time from the natriuresis.

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“…36 In another experimental renal hypertension model that used bilateral renal cellophane wrapping in rabbits, elevation of MAP was also due to increases in TPR from the earliest stage. 37 Evidence has been reported that volume factors influencing cardiac output and vasoconstriction factors influencing TPR can produce chronic hypertension independent of each other. 36 - 37 Our study of chronic intrarenal NE infusion in conscious rats has confirmed that renovascular hypertension can develop without a body-fluid volume-dependent stage.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic characterization of hypertension induced by chronic intrarenal or intravenous infusion of norepinephrine in conscious rats.

Kleinjans¹,

Smits²,

Essen³

et al. 1984

Hypertension

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SUMMARY The present study was designed to determine the hemodynamic changes underlying the hypertension induced by chronic intrarenal infusion of norepinephrine (NE) in conscious rats. NE was infused for a 5-day period intrarenally with osmotic minipumps via a chronic catheter in the right suprarenal artery at rates of 4 and 36 /*g-kg~'-hr~l or intravenously at a rate of 36 ^g-kg~'-hr~'. Control rats received a 1 ^ilhr" 1 intrarenal infusion of pyrogen-free 0.9% NaCl. In separate experiments, short-term effects were measured continuously during a 22-to 24-hour intrarenal infusion of 4 and 36 /xg NE-kg~'-hr~' or intravenous infusion of 36 ^.g NE-kg~'-hr~'. Intrarenal infusion of NE produced a more pronounced long-term hypertensive effect than infusion of the same dose intravenously. This hypertension was characterized by a rapid and sustained increase in total peripheral resistance index (TPRI). Despite of the initial renal vasoconstriction, specifically produced during the first 24 hours of intrarenal NE application, cardiac index (CD in parallel to stroke volume index (SVI) decreased significantly during intrarenal as well as during intravenous NE infusion. Furthermore, no signs of sodium retention were observed. Both rates of intrarenal NE infusion have been shown previously to produce a significant long-term increase in plasma potassium concentration, and the present study indicates that this is presumably the result of decreased urinary potassium output. It is concluded that chronic hypertension produced by intrarenal or intravenous infusion of NE is not volume-dependent. The relatively greater increase in TPRI during intrarenal NE infusion is attributed to vascular wall receptor sensitization by increased plasma potassium levels resulting from effects of intrarenally present NE on tubular cation exchange mechanisms. pressure regulation is widely accepted. The fundamental renal control mechanism is the pressure-diuresis/natriuresis system that counterbalances small alterations in arterial pressure by large changes in renal water and salt excretion.' 12 The level at which the renal hydraulic system controls arterial pressure is influenced by hormonal and neurogenic factors; any change in renal vascular resistance and tubular handling of fluid and electrolytes can result in a shift of this renal function curve setpoint to other levels of arterial pressure.

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The Present Status of the Autoregulation Theory of the Pathogenesis of Hypertension

Cited by 11 publications

References 20 publications

Effect of ouabain on hemodynamics in acute volume expanded hypertensive dogs

Effect of ouabain on hemodynamics in acute volume expanded hypertensive dogs

Contribution of the baroreflex afferent nerves to the production of vasoconstricted hypertension in volume-expanded dogs.

Hemodynamic characterization of hypertension induced by chronic intrarenal or intravenous infusion of norepinephrine in conscious rats.

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