Genetic epidemiology of essential hypertension

Gavras, Irène; Manolis, Athanasios; Gavras, Haralambos

doi:10.1038/sj.jhh.1000794

Cited by 17 publications

(10 citation statements)

References 53 publications

(64 reference statements)

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“…Spontaneously hemorrhaging rats represent an accurate model for human essential hypertension (EH). 16 Genetic studies 17 of both SHR 18 and EH 19,20 show a strong inherited predisposition to hypertension. On a molecular level SHR 21 and EH 22 have similar membrane defects in sodium transport.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Hypertension on the Response to Blood Loss in a Rodent Model

Sinert¹,

Guerrero²,

Quintana³

et al. 2000

Academic Emergency Medicine

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Abstract.Objective: Hypertensive patients having higher baseline peripheral resistance and sympathetic tone than normotensive patients may have aberrant responses to hemorrhage. In an attempt to further characterize this clinical observation, the authors compared the hemodynamic and metabolic responses to hemorrhage between spontaneously hypertensive rats (SHR) and normotensive rats (NTR). Methods: Twenty adult rats (10 NTR and 10 SHR) were anesthetized with althesin via the intraperitoneal route. Femoral arteries were cannulated by cutdown. Twelve (6 SHR and 6 NTR) rats underwent controlled catheter hemorrhage of 25% of their total blood volumes. Eight rats (4 SHR and 4 NTR) served as nonhemorrhage controls. Mean arterial pressure (MAP) and base excess (BE) were measured prehemorrhage and then every 15 minutes for the next 120 minutes. Data were reported as mean Ϯ standard error of the mean (SEM). Group comparisons were analyzed by ANOVA with repeated values post-hoc by Bonferroni. Statistical significance was defined by an alpha = 0.05. Results: Immediately after hemorrhage, the SHR group experienced a significantly (p < 0.001) greater drop in MAP of 70 Ϯ 4% in the SHR vs 40 Ϯ 6% in the NTR. Blood pressure in the NTR returned to control values 15 minutes after hemorrhage, but the SHR remained relatively hypotensive for the entire length of the experiment. Base excess in the SHR decreased significantly (p < 0.004) by 8.2 Ϯ 2 mmol/L from control values, as compared with no changes in BE for the NTR. Conclusions: The authors observed significant differences in the response to hemorrhage between hypertensive and normotensive rats. Hypertensive rats experienced a more profound hemorrhagic shock insult than normotensives for the same degree of blood loss.

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Section: Discussionmentioning

confidence: 99%

The Effect of Hypertension on the Response to Blood Loss in a Rodent Model

Sinert¹,

Guerrero²,

Quintana³

et al. 2000

Academic Emergency Medicine

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“…The SHR has been extensively used as a model to study human EH. 5 Both SHRs 25 and humans with EH 26 show a strong genetic predisposition to develop hypertension. Similar defects in membrane transport of sodium have been identified in SHRs 27 and EH patients.…”

Section: Clinical Relevancementioning

confidence: 99%

“…Essential hypertension is a polygenetic multifactorial disorder where multiple genes interact with each other and the environment. 26 The epidemiology of EH complication rates also shows a racial heterogenicity. African American populations have significantly higher complication rates of heart and renal disease from EH than whites.…”

Section: Limitationsmentioning

confidence: 99%

The Effect of Hypertension on Uncontrolled Hemorrhage in a Rodent Model

et al. 2002

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Section: Clinical Relevancementioning

confidence: 99%

The Effect of Hypertension on Uncontrolled Hemorrhage in a Rodent Model

Sinert

2002

Academic Emergency Medicine

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Patients with essential hypertension (EH) have higher mortality rates from hemorrhage. How the complex physiologic changes seen in EH affect the response to uncontrolled hemorrhage has yet to be adequately described. Objective: To test the null hypothesis that there would be no difference in the hemorrhage volumes and hemodynamic responses to uncontrolled hemorrhage between hypertensive rats (SHRs) and normotensive rats (WKYs). Methods: Twenty-four adult rats (12 WKYs and 12 SHRs) were anesthetized with althesin via the intraperitoneal route. The femoral artery was cannulated by cutdown for mean arterial pressure (MAP) measurement and blood gas sampling. Twelve rats (6 WKYs and 6 SHRs) underwent uncontrolled hemorrhage by 50% tail amputation. Twelve rats (6 WKYs and 6 SHRs) served as non-hemorrhage controls. The MAP, base excess (BE), and cumulative blood loss were measured pre-hemorrhage and then every 15 minutes post-hemorrhage for 90 minutes. Data were reported as mean Ϯ standard error of the mean. Comparisons between control and uncontrolled hemorrhage groups were analyzed by analysis of variance (ANOVA) with repeated-measures post-hoc testing by Bonferroni. Statistical significance was defined by an alpha = 0.05. Results: Mortality rates were significantly higher (p < 0.05) for the SHRs (100%) as compared with the WKYs (33%). Changes in time-averaged MAP post-hemorrhage were significantly greater (p < 0.001) in the SHR group (88 Ϯ 10 mm Hg) as compared with the WKY group (48 Ϯ 4 mm Hg). Hemorrhage volume was significantly lower (p = 0.02) in the SHR group (3.7 Ϯ 0.5 mL) as compared with the WKY group (6.1 Ϯ 0.7 mL). Conclusions: Hypertensive rats had a higher mortality rate than normotensives from a comparable vascular injury with lower hemorrhage volumes.

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Genetic epidemiology of essential hypertension

Cited by 17 publications

References 53 publications

The Effect of Hypertension on the Response to Blood Loss in a Rodent Model

The Effect of Hypertension on the Response to Blood Loss in a Rodent Model

The Effect of Hypertension on Uncontrolled Hemorrhage in a Rodent Model

The Effect of Hypertension on Uncontrolled Hemorrhage in a Rodent Model

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