Role of salt in the control of blood pressure in obesity and diabetes mellitus.

Tuck, Michael L.

doi:10.1161/01.hyp.17.1_suppl.i135

Cited by 29 publications

(10 citation statements)

References 32 publications

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“…Also, while the association between HT and obesity is well documented, the pathogenesis of increased blood pressure in the obese is poorly understood. Mechanisms such as hypervolemia causing increased cardiac output with failure of an appropriate reduction in systemic vascular resistance [17], stimulation of the renin–angiotensin–aldosterone system [18] and increased salt intake due to increased caloric intake [19] have been proposed. In our patient group, only age was an independent factor related to HT.…”

Section: Discussionmentioning

confidence: 99%

Duration of obesity is not a risk factor for type 2 diabetes mellitus, arterial hypertension and hyperlipidemia

Hekimsoy

Oktem

2003

Diabetes Obesity Metabolism

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Section: Discussionmentioning

confidence: 99%

Duration of obesity is not a risk factor for type 2 diabetes mellitus, arterial hypertension and hyperlipidemia

Hekimsoy

Oktem

2003

Diabetes Obesity Metabolism

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“…Santos et al reported salt sensitivity in streptozotocin (STZ)-treated diabetic rats, but that was after 8 weeks of diabetes. 10 There is stronger evidence for salt sensitivity of blood pressure in Type II diabetes 11,12 and in longstanding Type I diabetes after the onset of microalbuminuria, 13,14 but it is not known how salt intake affects blood pressure at the very earliest stages of Type I diabetes in humans or in animals.…”

Section: Introductionmentioning

confidence: 99%

Lack of Blood Pressure Salt‐sensitivity Supports a Preglomerular Site of Action of Nitric Oxide in Type I Diabetic Rats

Brands

Bell

Fleming

et al. 2007

Clin Exp Pharma Physio

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1. The relationship between sodium intake and blood pressure is affected differently by changes in angiotensin (Ang) II and preglomerular resistance, and this study measured that relationship to evaluate the link between nitric oxide and blood pressure early in diabetes. 2. Rats were chronically instrumented, placed on high-sodium (HS = 12 mEq/d) or low-sodium (LS = 0.07 mEq/d) intake diets and assigned to either vehicle- (V) or Nomega-nitro-L-arginine methyl ester- (L-NAME; L) treated groups. Mean arterial pressure (MAP) was measured 18 h/day for a 6-day control and 14-day streptozotocin diabetic period in each animal. 3. The MAP of the control period averaged 95 +/- 1 and 94 +/- 1 mmHg in the LSV and HSV rats and 116 +/- 2 and 124 +/- 1 mmHg in the LSL and HSL rats, respectively (LSL vs HSL was significant at P < 0.05). Diabetes increased MAP only in the LSL and HSL rats to 141 +/- 2 mmHg and 152 +/- 2, respectively, similar to our previous reports, and those respective 25 and 28 mmHg increases were a parallel shift in the pressure natriuresis relationship. However, the apparent difference between the LSL and HSL groups when compared was a parallel of the control MAP difference. Plasma renin activity (PRA) in the control period averaged 1.5 +/- 0.5 and 8.1 +/- 1.8 ng AI/mL per h in the HSV and LSV rats, and 0.8 +/- 0.2 and 2.8 +/- 0.5 ng AI/mL per h in the HSL and LSL rats, respectively, and increased similarly by 4.6-fold in the HSL and 4.8-fold in the LSL rats during diabetes. Glomerular filtration rate (GFR) increased in the vehicle but not the L-NAME-treated groups, consistent with our previous reports. 4. Thus, the hypertension caused by the onset of diabetes in L-NAME-treated rats was not salt-sensitive. The normal modulation of PRA by salt intake and the failure of GFR to increase are consistent with our hypothesis that nitric oxide may protect against hypertension early in diabetes by preventing preglomerular vasoconstriction by AngII.

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“…Counseling is tailored to individuals who are diabetic, 56–58 African American, 59, 60 recently diagnosed with hypertension, and/or have hypertensive relatives 61, 62 because these factors confer specific risks for worse health outcomes.…”

Section: Figurementioning

confidence: 99%

Open-label randomized trial of titrated disease management for patients with hypertension: Study design and baseline sample characteristics

Jackson

Weinberger

Kirshner³

et al. 2016

Contemporary Clinical Trials

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Despite the availability of efficacious treatments, only half of patients with hypertension achieve adequate blood pressure (BP) control. This paper describes the protocol and baseline subject characteristics of a 2-arm, 18-month randomized clinical trial of titrated disease management (TDM) for patients with pharmaceutically-treated hypertension for whom systolic blood pressure (SBP) is not controlled (≥140mmHg for non-diabetic or ≥130mmHg for diabetic patients). The trial is being conducted among patients of four clinic locations associated with a Veterans Affairs Medical Center. An intervention arm has a TDM strategy in which patients' hypertension control at baseline, 6, and 12 months determines the resource intensity of disease management. Intensity levels include: a low-intensity strategy utilizing a licensed practical nurse to provide bi-monthly, non-tailored behavioral support calls to patients whose SBP comes under control; medium-intensity strategy utilizing a registered nurse to provide monthly tailored behavioral support telephone calls plus home BP monitoring; and high-intensity strategy utilizing a pharmacist to provide monthly tailored behavioral support telephone calls, home BP monitoring, and pharmacist-directed medication management. Control arm patients receive the low-intensity strategy regardless of BP control. The primary outcome is SBP. There are 385 randomized (192 intervention; 193 control) veterans that are predominately older (mean age 63.5 years) men (92.5%). 61.8% are African American, and the mean baseline SBP for all subjects is 143.6mmHg. This trial will determine if a disease management program that is titrated by matching the intensity of resources to patients' BP control leads to superior outcomes compared to a low-intensity management strategy.

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Role of salt in the control of blood pressure in obesity and diabetes mellitus.

Cited by 29 publications

References 32 publications

Duration of obesity is not a risk factor for type 2 diabetes mellitus, arterial hypertension and hyperlipidemia

Duration of obesity is not a risk factor for type 2 diabetes mellitus, arterial hypertension and hyperlipidemia

Lack of Blood Pressure Salt‐sensitivity Supports a Preglomerular Site of Action of Nitric Oxide in Type I Diabetic Rats

Open-label randomized trial of titrated disease management for patients with hypertension: Study design and baseline sample characteristics

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