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We investigated the association of adipose tissue insulin resistance with blood pressure and hypertension incidence, comparing it with hepatic and skeletal muscle insulin resistance. The cross-sectional analysis included 6892 general health checkup examinees (mean age: 69.3 years; 51.3% women and 48.7% men) who had no cardiovascular disease. Of those, 3948 normotensive participants (mean age: 68.4 years; 54.8% women and 45.2% men) were enrolled in the retrospective cohort analysis. The adipose insulin resistance index (Adipo-IR) was calculated as the product of fasting serum insulin and free fatty acid levels. A high adipo-IR, high homeostasis model assessment of insulin resistance (HOMA-IR), and low Matsuda index were indicated based on the optimal cutoff values in a receiver operating characteristic curve analysis. Adipo-IR (β = 0.096, P < 0.001), HOMA-IR (β = 0.052, P < 0.001), and Matsuda index (β = −0.055, P < 0.001) were associated with systolic blood pressure in the cross-sectional analysis. Over a mean 5.3-year follow-up period, 1310 participants developed hypertension. A high adipo-IR (adjusted OR, 1.29; 95% CI, 1.11–1.51), but not HOMA-IR or Matsuda index, was significantly associated with the incidence of hypertension. Moreover, the combination of high adipo-IR with high HOMA-IR or low Matsuda index showed no higher odds of hypertension than a high adipo-IR alone. These results suggest that insulin resistance is associated with blood pressure control regardless of the tissue in which it occurs; however, the risk of hypertension is determined by insulin resistance in adipose tissue rather than in liver or muscle tissue.

IntroductionLittle is known about the risk of hypertension in patients with the early stage of type 2 diabetes. We investigated the risk of hypertension in participants with newly diagnosed type 2 diabetes and prediabetes.Research design and methodsThis is a retrospective cohort study consisting of 2136 middle-aged participants (1022 with normal fasting glucose/normal glucose tolerance (NFG/NGT), 418 with impaired fasting glucose (IFG), 466 with impaired glucose tolerance (IGT) and 230 with diabetes) and 3426 elderly participants (1762 with NFG/NGT, 599 with IFG, 781 with IGT, and 284 with diabetes). All participants underwent 75 g oral glucose tolerance tests at baseline.ResultsOver a median 59-month follow-up period, 459 middle-aged and 1170 elderly participants developed hypertension. In middle-aged participants, the odds of incident hypertension were significantly higher in those with IFG (OR 1.40; p=0.019), IGT (OR 1.49; p=0.004), and diabetes (OR 1.55; p=0.013) than those with NFG/NGT, which was no longer significant after adjustment for body mass index. Subgroup analysis showed that the risk of hypertension was significantly higher in diabetes than NFG/NGT only in participants without obesity. Conversely, obesity was a risk factor of hypertension only in those with IFG and NFG/NGT. In elderly participants, there was no difference in the risk of hypertension among the NFG/NGT, IFG, IGT and diabetes groups.ConclusionsThe risk of hypertension is modest in participants with newly diagnosed type 2 diabetes and prediabetes. Our findings suggest that the early stages of type 2 diabetes and prediabetes may be a key period for reducing hypertension, given the pronounced risk of hypertension in patients with diabetes reported in previous studies. In terms of reducing the risk for hypertension, obesity treatment might be advantageous in the early stages rather than the advanced stages of impaired glucose metabolism.

We evaluated data from 10,088 participants without cardiovascular disease (CVD) who underwent 75 g oral glucose tolerance tests and had more than four visits during the first 5 years following the test to investigate the association between impaired glucose metabolism and visit-to-visit blood pressure (BP) variability. Participants were classified into groups of normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and diabetes. Visit-to-visit BP variability was estimated for each individual using standard deviation (SD) and coefficients of variation (CV, defined as SD/mean). SDs and CVs of systolic BP (SBP) values were divided into quartiles. The samples falling in the highest quartile were considered as having high SD/CV. The adjusted odds ratio (OR) for high SD of SBP in the IFG (OR, 1.39; P<0.003), IGT (OR, 1.26; P<0.001), and diabetes (OR, 1.54; P<0.001) groups was significantly higher than that for high SD of SBP in the NGT group. Similarly, the OR for high CV of SBP in the IGT and diabetes groups was significantly higher than that for high CV of SBP in the NGT group. In participants without CVD, impaired glucose metabolism may modulate visit-to-visit BP variability.

Short-term blood pressure (BP) variability is an important cardiovascular risk factor. Whether patients with obstructive sleep apnea syndrome (OSAS) indeed display increased short-term BP variability and, if so, what is its underlying mechanism remain unclear. We compared the short-term BP variability between hypertensive patients with OSAS (OSAS group; n= 212) and those without OSAS (control group; n = 82) by examining data of 24-h ambulatory BP monitoring (ABPM) and investigated the effects of continuous positive airway pressure (CPAP) therapy on short-term BP variability in 37 hypertensive patients with OSAS. Short-term BP variability was calculated with the average real variability (ARV) of awake and sleep BP. ARVs of sleep systolic BP (SBP) and diastolic BP (DBP) were significantly higher in the OSAS group than in the control group. There was no significant difference in ARVs of awake SBP and DBP between the two groups. In the OSAS group, multiple regression analyses revealed that the body mass index (BMI) was an independent determinant for ARV of sleep DBP and that the lowest SpO2 was an independent determinant for ARVs of sleep SBP and sleep DBP. CPAP therapy decreased ARVs of sleep SBP and DBP. These results suggested that higher short-term BP variability during sleep is a characteristic feature of hypertensive patients with OSAS and that obesity and hypoxemia play essential roles in increasing short-term BP variability during sleep. CPAP therapy may improve exaggerated short-term BP variability during sleep in patients with OSAS.

Dopamine D2 receptors (D2Rs) are expressed in the kidney. It has not been determined whether D2Rs are involved in the mechanism of sodium handling and blood pressure (BP) control. The function of D2Rs was investigated in mice disrupted with D2R gene (D2KO mice). Six-week-old male D2KO mice and wild-type (WT) mice were fed high-salt (4% NaCl) or low-salt (0.01% NaCl) diets for 8 weeks. Before starting the metabolic diet, there were no significant differences in body weight, food consumption, and 24-h urine excretions of creatinine, sodium and potassium. The high-salt diet caused a significant elevation in systolic BP in D2KO mice but not in WT mice. Calculation of sodium and potassium balances revealed a significantly high level of sodium retention in D2KO mice placed on the high-salt diet. Twenty-four-hour urine norepinephrine excretions and heart rates, indicators of sympathetic activity, were not different in D2KO and WT mice on the high-salt diet. Administration of nemonapride, a specific D2-like receptor antagonist, to WT mice given 0.9% NaCl in drinking water caused suppression of urinary sodium excretion but had no effect in mice without salt loading. These results suggest that D2 receptors promote sodium excretion during a period of high salt intake. A defect in this mechanism may result in sodium-dependent BP elevation.

Hypertension is associated with vascular failure, such as increased arterial stiffness, endothelial dysfunction, and vascular smooth muscle dysfunction. The purpose of this study was to investigate the relationship between out-of-office blood pressure and vascular function in patients receiving antihypertensive drugs. We assessed out-of-office blood pressure, including daytime and night-time blood pressure, by home blood pressure monitoring and performed vascular function tests, including brachial-ankle pulse wave velocity (baPWV), flow-mediated vasodilation (FMD), and nitroglycerine-induced vasodilation (NID), in 169 patients receiving antihypertensive drugs, of whom 86 (50.9%) had normotension, 23 (13.6%) had isolated nocturnal hypertension (night-time systolic blood pressure ≥120 mm Hg), 26 (15.4%) had isolated daytime hypertension (daytime systolic blood pressure ≥135 mm Hg), and 34 (20.1%) had sustained hypertension (daytime and nocturnal hypertension). baPWV was significantly higher in patients with sustained hypertension than in those without sustained hypertension (1585 ± 257 cm/s in normotension; 1687 ± 267 cm/s in isolated nocturnal hypertension; 1688 ± 313 cm/s in isolated daytime hypertension; and 1923 ± 399 cm/s in sustained hypertension; P < 0.001). baPWV above the cutoff value of 1858 cm/s, derived from receiver operating characteristic curve analysis to diagnose patients with sustained hypertension, was significantly associated with sustained hypertension after adjustment of other confounding factors (odds ratio, 5.01; 95% confidence interval, 1.94-13.41; P < 0.001). In contrast, there was no significant association of home blood pressure status with FMD or NID in these patients. In patients receiving antihypertensive drugs, baPWV was significantly associated with sustained hypertension, whereas FMD and NID were impaired regardless of the home blood pressure status.

We have recently demonstrated that type 1A dopamine (D1A) receptor is expressed in the rat heart, but its function still remains unknown. In the present study, we investigated possible changes in the expression level and the distribution of the cardiac D1A receptor in the development of left ventricular hypertrophy in spontaneously hypertensive rats/Izumo strain (SHR/Izm) at the ages of 4, 8, and 20 weeks. We examined D1A receptor protein distribution by immunohistochemistry and gene expression by competitive polymerase chain reaction (competitive PCR). In SHR/Izm, compared with the age-matched Wistar Kyoto rats/ Izmo strain (WKY/Izm), blood pressure and heart/body weight ratio were significantly increased at 8 and 20 weeks. By immunohistochemistry, the D1A receptor was localized in cardiomyocytes and vascular smooth muscle cells of coronary arteries, but not in interstitial fibrotic tissue. D1A receptor distribution was not changed either by the strain or the age. Competitive PCR analysis showed that the D1A receptor mRNA level was significantly higher at 4 weeks than at 8 and 20 weeks in both strains of rats and that there was no significant difference in D1A receptor mRNA between SHR/Izm and WKY/Izm at any age ( 43.2 ± 10.4 attomol × 10−3/L v 43.1 ± 11.2 attomol × 10−3/L at 4 weeks, P = not significant, 3.9 ± 0.9 attomol × 10−3/L v 4.0 ± 1.3 attomol × 10−3/L at 8 weeks, P = not significant, 3.0 ± 1.2 attomol × 10−3/L v 1.9 ± 1.6 attomol × 10−3/L at 20 weeks, P = not significant). These results do not support the hypothesis that changes in D1A receptor expression are associated with the development of left ventricular hypertrophy in SHR.

Restriction fragment length polymorphisms of the vitamin D receptor gene have recently been reported to be associated with changes in bone mineral density. Alterations in systemic calcium balance and Ca-regulating hormones such as 1,25(OH)2 vitamin D3 and parathyroid hormone have been demonstrated in essential hypertension. We investigated the relationship between polymorphisms of the vitamin D receptor gene and systemic Ca metabolism in patients with essential hypertension and in normotensives. We compared 147 subjects with essential hypertension and 100 normotensive control subjects. The genotype distribution and derived allele frequencies for the vitamin D receptor gene were similar in the two groups (genotype bb/Bb/BB and allele B/b: 60.1/32.6/7.2 and 0.24/0.76 in hypertensives vs. 56.0/36.0/8.0 and 0.26/0.74 in normotensive subjects). Serum concentrations of total Ca in the bb, Bb, and BB groups were, respectively, 4.5+/-0.3 vs. 4.5+/-0.4 vs. 4.4+/-0.5 mmol/l in normotensives and 4.6+/-0.3 vs. 4.6+/-0.4 vs. 4.4+/-0.5 mmol/l in hypertensives. Ionized Ca levels were 1.17+/-0.04 vs. 1.16+/-0.04 vs. 1.15+/-0.04 mmol/l in normotensives and 1.16+/-0.04 vs. 1.16+/-0.04 vs. 1.14+/-0.05 mmol/l in hypertensives, respectively. These results indicate that the BB genotype of the vitamin D receptor gene is associated with lower serum Ca levels but is not a useful predictive marker for the development of essential hypertension in Japanese subjects.