Analysis of arterial pressure regulating systems in renal post-transplantation hypertension

Grisk, Olaf; Heukäufer, Matthias; Steinbach, Antje; Gruska, S; Rettig, Rainer

doi:10.1097/00004872-200401000-00030

Cited by 19 publications

(24 citation statements)

References 31 publications

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“…Possible mechanisms include: (1) the reninangiotensin-aldosterone system, (2) renal sodium and volume handling, (3) sympathorenal interactions, and (4) (enhanced) production or inadequate excretion of a hitherto unknown hypertensinogenic substance. In several studies, 15,18,27,30,33,34 we were able to demonstrate that the renin-angiotensin-aldosterone system is not stimulated in recipients of an SHRSP or SHR kidney. Interestingly, recipients of an SHRSP kidney had a lower 24-hour urinary aldosterone secretion, 15 and recipients of an SHR kidney had lower plasma aldosterone concentrations than recipients of a kidney from normotensive donors.…”

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 86%

“…Interestingly, recipients of an SHRSP kidney had a lower 24-hour urinary aldosterone secretion, 15 and recipients of an SHR kidney had lower plasma aldosterone concentrations than recipients of a kidney from normotensive donors. 18 From these and other observations, we hypothesized that recipients of an SHRSP or SHR kidney, respectively, may have a primary defect in renal sodium handling. In fact, when we challenged our rats with a dietary sodium load, recipients of an SHRSP kidney showed a decreased renal capacity to excrete the load.…”

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 93%

“…When radiotelemetric blood pressure recordings became available to us, it soon became clear that renal post-transplantation hypertension in recipients of an SHR kidney started to develop much earlier than thought previously (ie, within the very first days after transplantation and well before the removal of the second native kidney). 18 A recent reinvestigation of the issue revealed that overall sodium balances and plasma volumes were similar in recipients of an SHR kidney and in recipients of an F1 hybrid kidney despite a significantly higher blood pressure in the former group. 18 Sodium may affect blood pressure by causing volume expansion or by increasing vascular reactivity.…”

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 99%

“…18 A recent reinvestigation of the issue revealed that overall sodium balances and plasma volumes were similar in recipients of an SHR kidney and in recipients of an F1 hybrid kidney despite a significantly higher blood pressure in the former group. 18 Sodium may affect blood pressure by causing volume expansion or by increasing vascular reactivity. Therefore, we also investigated the contractile properties of recipient thirdorder mesenteric artery branches and of distal interlobar arteries from kidney grafts using a small-vessel wire myograph.…”

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 99%

“…There was no evidence for altered vasoconstrictory or vasodilatory properties in recipients of an SHR kidney versus recipients of an F1 hybrid kidney. 18 …”

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 99%

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The Kidney as a Determinant of Genetic Hypertension

Rettig

Grisk

2005

Hypertension

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Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 86%

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 93%

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 99%

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 99%

“…There was no evidence for altered vasoconstrictory or vasodilatory properties in recipients of an SHR kidney versus recipients of an F1 hybrid kidney. 18 …”

Section: Renal Mechanisms Of Hypertensionmentioning

confidence: 99%

See 3 more Smart Citations

The Kidney as a Determinant of Genetic Hypertension

Rettig

Grisk

2005

Hypertension

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Impaired coronary function in Wistar Ottawa Karlsburg W rats—a new model of the metabolic syndrome

Grisk

Frauendorf

Schlüter

et al. 2007

Pflugers Arch - Eur J Physiol

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The metabolic syndrome is associated with an increased risk for coronary heart disease. The underlying mechanisms are not well understood. The present study was designed to investigate coronary function in Wistar Ottawa Karlsburg W (WOKW) rats, a new animal model of the metabolic syndrome. The responses of coronary artery segments from WOKW and Dark Agouti (DA) control rats of different ages to several physiological vasoconstrictors and vasodilators were measured in a small vessel wire myograph, and potential mechanisms involved in the differential responses between the two strains were investigated. WOKW showed increased alpha(1)-adrenoceptor-mediated coronary constriction at 3 and 10 months of age, as well as seriously blunted beta-adrenoceptor-mediated coronary relaxation at 16 months of age. Responses to non-adrenergic agonists were not altered in WOKW compared to DA. The alpha(1)-adrenoceptor-mediated coronary constriction in WOKW was completely blocked by rho-kinase inhibition. Induced hyperinsulinemia did not cause increased alpha(1)-adrenoceptor-mediated coronary constriction or impaired beta-adrenoceptor-mediated coronary relaxation in DA. The association between blunted coronary beta-adrenoceptor responsiveness and the metabolic syndrome was confirmed in Zucker diabetic fatty rats. We conclude that the metabolic syndrome in WOKW rats is associated with impaired coronary function due to altered adrenoceptor sensitivity. The latter may contribute to inappropriately elevated coronary tone in insulin-resistant subjects, especially when sympathetic activity to the heart is increased.

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A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

Gildea

Lahiff

Sciver

et al. 2013

Clinica Chimica Acta

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Background Salt sensitivity (SS) of blood pressure (BP) affects 25% of adults, shares comorbidity with hypertension, and has no convenient diagnostic test. We tested the hypothesis that urine-derived exfoliated renal proximal tubule cells (RPTCs) could diagnose the degree of an individual's SS of BP. Methods Subjects were selected who had their SS of BP determined 5 y prior to this study (salt-sensitive: ≥7 mm Hg increase in mean arterial pressure (MAP) following transition from a random weekly diet of low (10 mmol/day) to high (300 mmol/day) sodium (Na+) intake, N = 4; inverse salt-sensitive (ISS): ≥7 mm Hg increase in MAP transitioning from a high to low Na+ diet, N = 3, and salt-resistant (SR): <7 mm Hg change in MAP transitioned on either diet, N = 5). RPTC responses to 2 independent Na+ transport pathways were measured. Results There was a negative correlation between the degree of SS and dopamine-1 receptor (D1R) plasma membrane recruitment (y = −0.0107x + 0.68 relative fluorescent units (RFU), R2 = 0.88, N = 12, P < 0.0001) and angiotensin II-stimulated intracellular Ca++ (y = −0.0016x + 0.0336, R2 = 0.7112, P < 0.001, N = 10) concentration over baseline. Conclusions Isolating RPTCs from urine provides a personalized cell-based diagnostic test of SS index that offers advantages over a 2-week controlled diet with respect to cost and patient compliance. Furthermore, the linear relationship between the change in MAP and response to 2 Na+ regulatory pathways suggests that an individual's RPTC response to intracellular Na+ is personalized and predictive.

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Analysis of arterial pressure regulating systems in renal post-transplantation hypertension

Cited by 19 publications

References 31 publications

The Kidney as a Determinant of Genetic Hypertension

The Kidney as a Determinant of Genetic Hypertension

Impaired coronary function in Wistar Ottawa Karlsburg W rats—a new model of the metabolic syndrome

A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: The virtual renal biopsy

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