Elevation of systolic blood pressure in an animal model of olanzapine induced weight gain

2006 ◽  
Vol 551 (1-3) ◽  
pp. 112-115 ◽  
Author(s):  
Basanagouda M. Patil ◽  
Nagaraj M. Kulkarni ◽  
Banappa S. Unger
2015 ◽  
Vol 7 (3) ◽  
pp. 306-313 ◽  
Author(s):  
S. Sandboge ◽  
C. Osmond ◽  
E. Kajantie ◽  
J. G Eriksson

Previous studies suggest that the inverse association between birth weight and adult blood pressure amplifies with age. Rapid childhood growth has also been linked to hypertension. The objective of this study was to determine whether the association between childhood growth and adult blood pressure amplifies with age. The study comprised 574 women and 462 men from the Helsinki Birth Cohort Study who attended a clinical study in 2001–2004 and a follow-up in 2006–2008. Mean age at the clinic visits was 61.5 and 66.4 years, respectively. Blood pressure was measured at both occasions. Conditional growth models were used to assess relative weight gain and linear growth. We studied the associations between conditional growth and blood pressure as well as the presence of hypertension. Relative weight gain and linear growth between ages 2 and 11 years were inversely associated with systolic blood pressure at mean age 66.4 years, after adjustment for sex, blood pressure at mean age 61.5 years, as well as other covariates. A one s.d. increase in linear growth between 2 and 11 years was associated with an OR of 0.61 for hypertension at mean age 66.4 years. Contrary to previous studies, we have shown an inverse association between childhood growth and adult blood pressure. There were, however, no associations between childhood growth and systolic blood pressure at mean age 61.5 years indicating that the beneficial effects of a more rapid than expected childhood growth might become more apparent with increasing age.


Hypertension ◽  
2016 ◽  
Vol 67 (2) ◽  
pp. 301-308 ◽  
Author(s):  
Wei Perng ◽  
Sheryl L. Rifas-Shiman ◽  
Michael S. Kramer ◽  
Line K. Haugaard ◽  
Emily Oken ◽  
...  

In recent years, the prevalence of hypertension and prehypertension increased markedly among children and adolescents, highlighting the importance of identifying determinants of elevated blood pressure early in life. Low birth weight and rapid early childhood weight gain are associated with higher future blood pressure. However, few studies have examined the timing of postnatal weight gain in relation to later blood pressure, and little is known regarding the contribution of linear growth. We studied 957 participants in Project Viva, an ongoing US prebirth cohort. We examined the relations of gains in body mass index z-score and length/height z-score during 4 early life age intervals (birth to 6 months, 6 months to 1 year, 1 to 2 years, and 2 to 3 years) with blood pressure during mid-childhood (6–10 years) and evaluated whether these relations differed by birth size. After accounting for confounders, each additional z-score gain in body mass index during birth to 6 months and 2 to 3 years was associated with 0.81 (0.15, 1.46) and 1.61 (0.33, 2.89) mm Hg higher systolic blood pressure, respectively. Length/height gain was unrelated to mid-childhood blood pressure, and there was no evidence of effect modification by birth size for body mass index or length/height z-score gain. Our findings suggest that more rapid gain in body mass index during the first 6 postnatal months and in the preschool years may lead to higher systolic blood pressure in mid-childhood, regardless of size at birth. Strategies to reduce accrual of excess adiposity during early life may reduce mid-childhood blood pressure, which may also impact adult blood pressure and cardiovascular health.


2020 ◽  
Vol 318 (2) ◽  
pp. H252-H263 ◽  
Author(s):  
L. J. Renshall ◽  
E. C. Cottrell ◽  
E. Cowley ◽  
C. P. Sibley ◽  
P. N. Baker ◽  
...  

Fetal growth restriction (FGR), where a fetus fails to reach its genetic growth potential, affects up to 8% of pregnancies and is a major risk factor for stillbirth and adulthood morbidity. There are currently no treatments for FGR, but candidate therapies include the phosphodiesterase-5 inhibitor sildenafil citrate (SC). Randomized clinical trials in women demonstrated no effect of SC on fetal growth in cases of severe early onset FGR; however, long-term health outcomes on the offspring are unknown. This study aimed to assess the effect of antenatal SC treatment on metabolic and cardiovascular health in offspring by assessing postnatal weight gain, glucose tolerance, systolic blood pressure, and resistance artery function in a mouse model of FGR, the placental-specific insulin-like growth factor 2 (PO) knockout mouse. SC was administered subcutaneously (10 mg/kg) daily from embryonic day (E)12.5. Antenatal SC treatment did not alter fetal weight or viability but increased postnatal weight gain in wild-type (WT) female offspring ( P < 0.05) and reduced glucose sensitivity in both WT ( P < 0.01) and P0 ( P < 0.05) female offspring compared with controls. Antenatal SC treatment increased systolic blood pressure in both male (WT vs. WT-SC: 117 ± 2 vs. 140 ± 3 mmHg, P < 0.0001; P0 vs. P0-SC: 113 ± 3 vs. 140 ± 4 mmHg, P < 0.0001; means ± SE) and female (WT vs. WT-SC: 121 ± 2 vs. 140 ± 2 mmHg, P < 0.0001; P0 vs. P0-SC: 117 ± 2 vs. 144 ± 4 mmHg, P < 0.0001) offspring at 8 and 13 wk of age. Increased systolic blood pressure was not attributed to altered mesenteric artery function. In utero exposure to SC may result in metabolic dysfunction and elevated blood pressure in later life. NEW & NOTEWORTHY Sildenafil citrate (SC) is currently used to treat fetal growth restriction (FGR). We demonstrate that SC is ineffective at treating FGR, and leads to a substantial increase systolic blood pressure and alterations in glucose homeostasis in offspring. We therefore urge caution and suggest that further studies are required to assess the safety and efficacy of SC in utero, in addition to the implications on long-term health.


2015 ◽  
Vol 212 (4) ◽  
pp. 499.e1-499.e12 ◽  
Author(s):  
Jessica R. Walter ◽  
Wei Perng ◽  
Ken P. Kleinman ◽  
Sheryl L. Rifas-Shiman ◽  
Janet W. Rich-Edwards ◽  
...  

1995 ◽  
Vol 268 (2) ◽  
pp. H646-H652 ◽  
Author(s):  
S. A. Klarr ◽  
R. F. Keep ◽  
A. L. Betz

Although it has long been established that cerebrospinal fluid potassium concentration (CSF [K]) is very tightly regulated, it has been reported that rats made hypertensive by central infusions of aldosterone have significantly lower CSF [K] compared with normotensive controls. We investigated whether reduced CSF [K] is also present in another animal model of hypertension, the deoxycorticosterone acetate (DOCA)-salt rat, and we hypothesized that chronic intracerebroventricular (IVT) infusion of potassium with miniosmotic pumps might attenuate the rise in blood pressure observed in these rats. DOCA-salt rats without IVT infusions or with control CSF infusions (0.5 microliter/h of 2.9 mM K for 2 wk) had a significantly increased systolic blood pressure and a significantly lower CSF [K] compared with their respective sham groups. In contrast, DOCA-salt rats receiving IVT infusions with elevated [K] (10, 30, or 150 mM) had significantly lower blood pressures compared with those receiving control CSF. They also did not exhibit decreased CSF [K] compared with their respective sham groups. At 10 and 150 mM K, the blood pressure rise in DOCA-salt rats was not significantly different from shams. At 30 mM K, there was a slight, but significant, increase in blood pressure in the DOCA-salt rats compared with their shams, but this rise was still much less than in DOCA-salt rats infused with 2.9 mM K. Infusions with elevated [K] had no effect on blood pressure in the sham animals. These studies suggest that altered brain potassium homeostasis may play an important role in the development of DOCA-salt hypertension.


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