Vascular responses of the perfused intestine to vasoactive agents during the development of two-kidney, one-clip Goldblatt hypertension in dogs.

Greenberg, S

doi:10.1161/01.res.48.6.895

Cited by 10 publications

(3 citation statements)

References 34 publications

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“…Previous studies have found that rabbits with renal artery stenosis exhibit pressor hyperresponsiveness to norepinephrine (5,6) and to vasopressin (7) prior to the development of hypertension. Similar results have also been reported in dogs (8,9). The perturbations that occur within the kidney following renal artery stenosis must be detected by receptors or sensors within the kidney; the resulting signal must then leave the kidney to be expressed ultimately as increased responsiveness of the smooth muscle cells of the arterioles.…”

supporting

confidence: 81%

Pressor Responsiveness in Renal Prehypertensive Rabbits with a Denervated Kidney

Johnson

et al. 1985

Experimental Biology and Medicine

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Norepinephrine was infused iv at several doses into four groups of conscious rabbits (six per group), and the pressor responses were recorded. The groups were 3-day sham-operated rabbits; 3-day, two-kidney rabbits with unilateral renal artery stenosis (RAS); 3-day, two-kidney rabbits with unilateral renal denervation; and 3-day, two-kidney rabbits with unilateral renal denervation plus RAS of the denervated kidney. The rabbits with RAS of an innervated kidney and those with RAS of a denervated kidney had the same pressor responses to norepinephrine, which were greater than the pressor responses in the sham-operated rabbits or in the rabbits with a denervated kidney but without RAS. Four additional groups of similarly prepared rabbits were infused with norepinephrine at 800 ng/min/kg body wt, and mean arterial pressure and cardiac output were determined before and during norepinephrine infusion. The rabbits with RAS of an innervated or of a denervated kidney had greater increases in total peripheral resistance as well as in mean arterial pressure during norepinephrine infusion than did the two groups of rabbits without RAS. This indicated that the rabbits with RAS also had increased vascular responses to norepinephrine. The concentration of norepinephrine in six denervated kidneys was extremely low as compared to that of six innervated kidneys. Because renal denervation did not diminish pressor and vascular hyperresponsiveness in 3-day RAS rabbits, the signal that originates in the kidney following RAS and that results ultimately in pressor and vascular hyperresponsiveness is not mediated by renal nerves.

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confidence: 81%

Pressor Responsiveness in Renal Prehypertensive Rabbits with a Denervated Kidney

Johnson

et al. 1985

Experimental Biology and Medicine

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“…2K1C is a well-established hypertension animal model. This model has been used for several decades (64)(65)(66)(67)(68), and the authors of the present study have used this model in a previous study (69). In this model, not only is the blood level of Ang II increased, the local tissue levels of Ang II are also enhanced.…”

Section: Discussionmentioning

confidence: 94%

TRPM8 downregulation by angiotensin II in vascular smooth muscle cells is involved in hypertension

Huang

Zhang

et al. 2017

Molecular Medicine Reports

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Angiotensin II (Ang II)-induced injury of vascular smooth muscle cells (VSMCs) serves an important role in hypertension and other cardiovascular disorders. Transient receptor potential melastatin 8 (TRPM8) is a thermally‑regulated Ca2+‑permeable channel that is activated by reduced body temperature. Although several recent studies have revealed the regulatory effect of TRPM8 in vascular tone and hypertension, the precise role of TRPM8 in dysfunction of vascular smooth muscle cells (VSMCs) induced by Ang II remains elusive. In the present study, the possible function of TRPM8 in Ang II‑induced VSMCs malfunction in vivo and in vitro was investigated. In the aortae from rats that had undergone a two‑kidney one‑clip operation, which is a widely‑used renovascular hypertension model, the mRNA and protein levels of TRPM8 were reduced. In addition, exogenous Ang II treatment decreased TRPM8 mRNA and protein expression levels in primary cultures of rat VSMCs. TRPM8 activation by menthol, a pharmacological agonist, in VSMCs, significantly attenuated the Ang II‑induced increase in reactive oxygen species and H2O2 production. In addition, TRPM8 activation reduced the Ang II‑induced upregulation of NADPH oxidase (NOX) 1 and NOX4 in VSMCs. Furthermore, TRPM8 activation relieved the Ang II‑induced activation of ras homolog gene family, member A‑rho associated protein kinase 2 and janus kinase 2 signaling pathways in VSMCs. In conclusion, the results presented in the current study indicated that TRPM8 downregulation by Ang II in VSMCs may be involved in hypertension.

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“…There is ample evidence showing that vascular hyperreactivity occurs prior to the elevation of BP in twokidney, one clip (2K1C) Goldblatt hypertension, 15 one-kidney, one clip (1K1C) hypertension, 16 DOCAsalt hypertension, 17 and figure 8 ligature hypertension. 18 It was also shown that vascular hyperreactivity preceded the onset of hypertension in S rats.…”

Section: Discussionmentioning

confidence: 99%

Hypertension-producing factor in serum of hypertensive Dahl salt-sensitive rats.

Hirata¹,

Tobian²,

Simon³

et al. 1984

Hypertension

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SUMMARY To investigate whether serum in hypertensive Dahl salt-sensitive rats (S rats) contains a hypertensinogenic substance, we examined the effects of repeated injections of serum from such S rats on blood pressure (BP) and pressor responses. Serum was collected from either hypertensive or normotensive S rats (fed an 8% or 0.11% NaCI diet, respectively) and injected into uninephrectomized recipient S rats for 2 weeks (0.45 ml, twice a day, i.v.). Serum from hypertensive rats injected for 14 days significantly increased BP by 14 mm Hg (143 vs 129, p < 0.05), pressor responses to angiotensin II (ANGII) by 45% (p < 0.005), pressor responses to norepinephrine (NE) by 38% (p < 0.025), and Na concentration in the aortic wall of recipient rats by 5.9% (p < 0.05), compared to the effects of the injection of serum from normotensive S rats. These results imply that hypertensive S serum contains a hypertensinogenic substance and that this serum factor produces a mild hypertension in the recipient rats and also contributes importantly to the hypertension in donor S rats. Dahl salt-resistant rats (R rats) on either 8% or 0.11% NaCI had normal BP. Their sera produced no differences in BP or in pressor responses in recipient rats. Hence 8% NaCI, which produced no hypertension, also induced no hypertensinogenic serum factors in R rats. We sought to determine whether nephrectomy would alter these humoral factors. The BP averaged 139 mm Hg in rats receiving normotensive sham-nephrectomized S serum vs 154 in those receiving hypertensive shamnephrectomized S serum, 15 mm Hg higher (p < 0.05). ANGII and NE pressor responses were uniformly higher in rats receiving hypertensive sham-nephrectomized S serum by 32% (p < 0.05) and by 36% (p < 0.025), respectively. In contrast, among nephrectomized rats there were no significant differences between rats receiving hypertensive S serum vs normotensive S serum. Removal of kidneys appeared to eliminate the hypertensinogenic factors, which suggests that they either come from the kidney or are strongly influenced by the kidney. (Hypertension 6: 709-716, 1984) KEY WORDS tissue sodium blood pressure nephrectomy pressor response NaCI hypertension angiotensin II • norepinephrine S LOWLY acting hypertensinogenic humoral factors have been reported in various kinds of experimental and human essential hypertension. Hypertension in Dahl salt-sensitive rats (S rats) also seems to be at least partly due to an uncommon humoral factor. Dahl and his coworkers 1 showed that saltresistant rats (R rats) became hypertensive when they were united in parabiosis to S rats on a high NaCI diet. A previous study in this laboratory 2 also demonstrated that perfusion of blood from hypertensive S rats increased the vascular resistance of isolated hindquarters from R rats. It was also demonstrated in this laborato- ry 3 that some circulating humoral factors in S rats halved the rate of sodium excretion by an isolated kidney from normal Sprague-Dawley rats. Although the characteristics of these humoral factors remain ...

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Vascular responses of the perfused intestine to vasoactive agents during the development of two-kidney, one-clip Goldblatt hypertension in dogs.

Cited by 10 publications

References 34 publications

Pressor Responsiveness in Renal Prehypertensive Rabbits with a Denervated Kidney

Pressor Responsiveness in Renal Prehypertensive Rabbits with a Denervated Kidney

TRPM8 downregulation by angiotensin II in vascular smooth muscle cells is involved in hypertension

Hypertension-producing factor in serum of hypertensive Dahl salt-sensitive rats.

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