Renal function reserve and sodium sensitivity in essential hypertension

Sanai, Toru; Kimura, Genjiro

doi:10.1016/s0022-2143(96)90117-1

Cited by 32 publications

(23 citation statements)

References 37 publications

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“…We previously investigated the glomerular haemodynamics using the pressure-natriuesis relationship in non-sodium sensitive and sodium sensitive type of essential hypertension, and demonstrated that reduced whole kidney ultrafiltration coefficient was the principal mechanism of sodium sensitivity. 10 Since HOMA insulin resistance index did not differ between non-sodium sensitive and sodium sensitive subjects, enhanced tubular sodium reabsorption by insulin resistance might not be the major determinant of sodium sensitivity. In fact, our study showed significant but weak relationships among sodium sensitivity, insulin resistance and tubular sodium reabsorption, indicating that the sodium sensitivity of BP is determined only in part by enhanced tubular sodium reabsorption in essential hypertension, while mostly by reduced ultrafiltration coefficient.…”

Section: Discussionmentioning

confidence: 93%

“…Patients whose 24-h average of mean arterial pressure was lowered by more than 10% by sodium restriction were assigned to the sodium sensitive group based on Bartter's original definition, 3,4 the remaining patients were assigned to the non-sodium sensitive group. In addition, sodium sensitivity index was calculated as the ratio of the change in mean arterial pressure over the change in urinary sodium excretion rate induced by sodium restriction, which was the reciprocal of the slope of the pressure natriuresis curve, 1,2,10,15,16,[30][31][32] and which represented how much BP was affected by each mmol of sodium intake per day altered in the steady state. 1,2 Plasma glucose and insulin response during a standard oral glucose tolerance test (OGTT) were determined in all subjects on a regular sodium diet.…”

Section: Study Protocolmentioning

confidence: 99%

“…1 In fact, we quantitatively estimated glomerular pressure elevated in this type of essential hypertension. 1,10 Microalbuminuria, a marker of glomerular capillary hypertension, 5,11 is now considered as a risk predictor for cardiovascular morbidity. [12][13][14] We also showed that BP failed to fall during the night in sodium sensitive type of essential hypertension, and they manifested as nondippers, 15,16 which were associated with more serious hypertensive end-organ damage including silent cerebrovascular infarction, left ventricular hypertrophy and microalbuminuria, than dippers whose BP Correspondence: Dr Genjiro Kimura, Chief, Division of Nephrology, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan Received 31 August 1998; revised 8 December 1998; accepted 24 December 1998 sodium sensitive and sodium sensitive groups.…”

Section: Introductionmentioning

confidence: 99%

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Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension

et al. 1999

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We recently showed that cardiovascular morbidity was higher in sodium sensitive type of essential hypertension than in the non-sodium sensitive type. It was examined whether sodium sensitivity was associated with insulin resistance, an important atherosclerotic cardiovascular risk factor in essential hypertension. Fiftythree patients with essential hypertension, who had normal (n ‫؍‬ 12) and impaired (n ‫؍‬ 41) glucose tolerance, were placed on high (12-15 g NaCl/day) and low (1-3 g) sodium diets for 1 week each to determine sodium sensitivity. Fasting plasma glucose and insulin concentrations were measured on a regular sodium diet. The homeostasis model assessment insulin resistance index (fasting glucose [mmol/L] ؋ fasting insulin [mU/L]/22.5) was 1.40 ؎ 0.10 and 1.47 ؎ 0.14 in non-

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Section: Discussionmentioning

confidence: 93%

Section: Study Protocolmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension

et al. 1999

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“…In addition to the non-dipper pattern, the salt sensitivity of BP is closely linked to glomerular capillary hypertension 28,46,60 and insulin resistance. [61][62][63][64][65][66] The non-dipper pattern, 67-73 microalbuminuria 74,75 (a marker for glomerular capillary hypertension), 76,77 insulin resistance and metabolic syndrome [78][79][80][81] are all known to be strong risk factors for cardiovascular events.…”

Section: Salt Sensitivity and Strokementioning

confidence: 99%

Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

2010

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In healthy subjects, blood pressure (BP) drops by 10-20% during the night. Conversely, in patients with the salt-sensitive type of hypertension or chronic kidney disease, nighttime BP does not fall, resulting in an atypical pattern of circadian BP rhythm that does not dip. This pattern is referred to as the 'non-dipper' pattern. Loss of renal functional reserve, due to either reduced ultrafiltration capacity or enhanced tubular sodium reabsorption, induces the salt-sensitive type of hypertension. When salt intake is excessive in patients with salt-sensitive hypertension, the defect in sodium excretory capability becomes evident, resulting in elevated BP during the night. This nocturnal hypertension compensates for diminished natriuresis during the daytime and enhances pressure natriuresis during the night. Nocturnal hypertension and the non-dipper pattern of circadian BP rhythm cause cardiovascular events. When excess salt intake is loaded in patients who are in a salt-sensitive state, glomerular capillary pressure is also elevated, resulting in glomerular sclerosis and eventual renal failure. In this way, salt sensitivity and excess salt intake contribute to both cardiovascular and renal damage at the same time. We propose that salt sensitivity of BP and excess salt intake have important roles in the genesis of the cardiorenal connection. Salt sensitivity and circadian rhythm of BP are the keys to understanding the connections between cardiovascular and renal complications.

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“…Thus, postural change in systemic haemodynamics would not probably play a key role in the difference of the postural changes in natriuresis patterns between dippers and non-dippers. We showed previously that nocturnal fall in BP [8][9][10] and renal function reserve in response to chronic protein load 19 was impaired in salt-sensi-…”

Section: Discussionmentioning

confidence: 95%

Circadian rhythm and postural change in natriuresis in non-dipper type of essential hypertension

et al. 2001

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Recently we found that, in non-dipper type of essential hypertensive patients who showed the lack of nocturnal fall in blood pressure, circadian rhythm of urinary sodium excretion rate was disturbed. In the present study we examined whether postural change in natriuresis is also disturbed in non-dippers. Sixteen inpatients with essential hypertension were maintained on a relatively high sodium diet containing 10 to 12 g of NaCl per day for 8 days. On the 7th day of the study period, 24-h ambulatory blood pressures were measured, and 5-7th days urinary samples were collected for both daytime and night-time. On the last day of the study period, patients stood for 2 h and then lay down for 2 h. Urinary volume and excretion rates of creatinine and sodium

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Renal function reserve and sodium sensitivity in essential hypertension

Cited by 32 publications

References 37 publications

Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension

Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension

Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

Circadian rhythm and postural change in natriuresis in non-dipper type of essential hypertension

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