Non-modulating hypertension. A subset of sodium-sensitive hypertension.

Williams, Gordon H.; Hollenberg, Norman K.

doi:10.1161/01.hyp.17.1_suppl.i81

Cited by 62 publications

(39 citation statements)

References 24 publications

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“…31 However, individuals with non-modulating hypertension do not show increased renal blood flow when sodium intake is increased. 31 Therefore, they would retain sodium and water, which could underlie their salt sensitivity. 31 Individuals with nonmodulating hypertension most often have normal or high renin levels.…”

Section: Non-modulating Hypertensionmentioning

confidence: 99%

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Aldosterone-to-renin ratio and home blood pressure in subjects with higher and lower sodium intake: the Ohasama Study

Satoh

Kikuya

Hara³

et al. 2010

Hypertens Res

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Aldosterone-to-renin ratio (ARR) is used to screen primary hyperaldosteronism. We investigated the association between ARR and the prevalence of hypertension using home blood pressure (HBP) measurements in community residents stratified for long-term habitual dietary sodium intake. We obtained HBP and conventional blood pressure (CBP) data for 514 participants aged X35 years not receiving antihypertensive treatment in the general population of Ohasama (mean age: 59.7 ± 10.8 years; 71.2% women). A standardized method was used to calculate habitual sodium intake from a food-frequency questionnaire. The prevalence of HBP hypertension (X135/85 mm Hg) and CBP hypertension (X140/90 mm Hg) were 12.6 and 20.2%, respectively. The median plasma renin activity (PRA), plasma aldosterone concentration (PAC) and ARR were 1.1 ng ml -1 h -1 , 6.4 ng per 100 ml and 5.5 ng per 100 ml per ng ml -1 h -1 , respectively. After adjustment for possible confounding factors, each 1 s.d. increase in logARR was associated with the prevalence of HBP hypertension (odds ratio 1.37; P¼0.04), but not with the prevalence of CBP hypertension (P¼0.2). The association of ARR with HBP hypertension was strengthened for subjects with high sodium intake (greater than or equal to the median of 4822 mg day -1 ), whereas it became nonsignificant for those with low sodium intake (interaction P¼0.03). Among subjects with high sodium intake, HBP hypertensives had significantly lower PRA than normotensives, despite no differences in PAC. In conclusion, relative aldosterone excess or low-renin hypertension may have an important role in HBP hypertension in the general population with high sodium intake.

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Section: Non-modulating Hypertensionmentioning

confidence: 99%

“…31 Individuals with nonmodulating hypertension most often have normal or high renin levels. 31 Thus, it is less likely that non-modulating hypertension contributed to our results of HBP hypertension with high sodium intake.…”

Section: Non-modulating Hypertensionmentioning

confidence: 99%

Aldosterone-to-renin ratio and home blood pressure in subjects with higher and lower sodium intake: the Ohasama Study

Satoh

Kikuya

Hara³

et al. 2010

Hypertens Res

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“…This finding is in agreement with some previous data suggesting a high prevalence of disturbances in glucose metabolism in non-modulators and supports the hypothesis that the non-modulating phenotype is due to different genetic traits predisposing individuals to hypertension. 4 Similarly, the presence of disturbances in glucose metabolism suggests that hypertension itself represents only one of the multiple risk factors evoked by different genes involved in the non-modulating phenotype.…”

Section: Renal and Hormonal Responses To Angiotensin IImentioning

confidence: 99%

Atrial natriuretic peptide in non-modulating essential hypertension.

et al. 1993

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To evaluate the atrial natriuretic peptide response to angiotensin II (Ang II) infusion in non-modulating hypertension, we studied 31 men with essential hypertension. These patients were subdivided into groups of low renin patients (n=8), non-modulators (R=11), and modulators 0 = 12) according to their renin profile and ability to modulate renin and aldosterone responses to a graded infusion of Ang II (1.0 and 3.0 ng/kg per minute) on a low Na + intake (10 mmol Na + per day). During basal conditions, plasma atrial natriuretic peptide was higher (p<0.05) in low renin patients (1634 ±2.67 fmol/mL) than in both modulators (10.59±4.29 fmol/mL) and non-modulators (9.85±2.64 fmol/mL). During Ang II infusion, plasma atrial natriuretic peptide significantly increased in both low renin (27.67±2.61 fmol/mL at 60 minutes, p<0.01) and modulating (20J6±3.07 fmol/mL at 60 minutes, p<0.05) patients, whereas it did not change in non-modulators (13.94±439 fmol/mL, NS). After 5 days on a high sodium intake (200 mmol Na + per day), plasma atrial natriuretic peptide rose in modulating (20.61 ±2Jl fmol/mL, p<0.01 versus low sodium intake), non-modulating (20.11±6.48 fmol/mL,p<0.01 versus low sodium intake), and low renin (26.13±3.81 fmol/mL, p<0.001 versus low sodium intake) hypertensive patients. When the Ang II infusion was repeated with a high sodium intake, plasma atrial natriuretic peptide increased again in low renin and modulating patients, whereas it did not change in non-modulators. Therefore, these data indicate that an impaired atrial natriuretic peptide responsiveness to Ang II that is not dependent on Na 1 indicated the lack of renal blood flow increase in response to dietary salt loading in some essential hypertensive patients. Then, an impaired aldosterone response to acute volume depletion was described by Williams et al 2 in a similar subgroup of hypertensive patients. At present, other characteristics of non-modulating hypertension have been described (see References 3 and 4 for review), including an increased blood pressure sensitivity to dietary salt intake 5 and decreased I) renal blood flow response to both angiotensin II (Ang II) and sodium loading, 5 -6 2) aldosterone response to Ang II,6 3) renin suppression after both Ang IP and saline infusions, 8 and 4) sodium excretion after sodium loading.9 Because an impaired responsiveness to Ang II of the adrenal gland and kidney seems to determine the hormonal and hemodynamic characteristics of nonmodulators, a tissue refractoriness to Ang II has been suggested as the primum movens of non-modulating hypertension (see References 3 and 4 for review). Address for correspondence: Claudio Ferri, MD, Universita "La Sapienza," Istituto di I Clinica Medica, Fondazione Andrea CesaJpino, 00161 Rome, Italy.Received November 3, 1992; accepted in revised form January 25, 1993. As is well known, atrial natriuretic peptide (ANP) is a natriuretic, diuretic, and vasorelaxant cardiac hormone (see Reference 10 for review) synthesized and secreted by atrial myocytes in response to a...

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“…However, the underlying mechanism of how salt intake induces hypertension is not yet clearly understood. It has been demonstrated that a high salt intake in hypertensive patients enhances sympathetic nerve activity and disturbs the renin-angiotensin system, leading to an increase in peripheral vascular resistance (Fujita et al, 1980;Williams & Hollenberg, 1991). In Dahl salt-sensitive hypertensive rats, a high salt diet has been shown to impair endothelium-dependent relaxations induced by a variety of vasodilators (LuÈ scher et al, 1987;Raij et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of vascular soluble guanylate cyclase induced by high salt intake in spontaneously hypertensive rats

Kagota

Tamashiro

Yamaguchi

et al. 2001

British J Pharmacology

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1 Cyclic guanosine monophosphate (cyclic GMP)-mediated mechanism plays an important role in vasodilatation and blood pressure regulation. We investigated the e ects of high salt intake on the nitric oxide (NO) ± cyclic GMP signal transduction pathway regulating relaxation in aortas of spontaneously hypertensive rats (SHR). 2 Four-week-old SHR and normotensive Wistar-Kyoto rats (WKY) received a normal salt diet (0.3% NaCl) or a high salt diet (8% NaCl) for 4 weeks. 3 In aortic rings from SHR, endothelium-dependent relaxations in response to acetylcholine (ACh), adenosine diphosphate (ADP) and calcium ionophore A23187 were signi®cantly impaired by the high salt intake. The endothelium-independent relaxations in response to sodium nitroprusside (SNP) and nitroglycerin were also impaired, but that to 8-bromo-cyclic GMP remained unchanged. On the other hand, high salt diet had no signi®cant e ects on the relaxations of aortic rings from WKY. 4 In aortas from SHR, the release of NO stimulated by ACh was signi®cantly enhanced, whereas the production of cyclic GMP induced by either ACh or SNP was decreased by the high salt intake. 5 Western blot analysis showed that the protein level of endothelial NO synthase (eNOS) was slightly increased, whereas that of soluble guanylate cyclase (sGC) was dramatically reduced by the high salt intake. 6 These results indicate that in SHR, excessive dietary salt can result in downregulation of sGC followed by decreased cyclic GMP production, which leads to impairment of vascular relaxation in responses to NO. It is notable that chronic high salt intake impairs the sGC/cyclic GMP pathway but not the eNOS/NO pathway.

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Non-modulating hypertension. A subset of sodium-sensitive hypertension.

Cited by 62 publications

References 24 publications

Aldosterone-to-renin ratio and home blood pressure in subjects with higher and lower sodium intake: the Ohasama Study

Aldosterone-to-renin ratio and home blood pressure in subjects with higher and lower sodium intake: the Ohasama Study

Atrial natriuretic peptide in non-modulating essential hypertension.

Downregulation of vascular soluble guanylate cyclase induced by high salt intake in spontaneously hypertensive rats

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