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Inherited risk plus prenatal insult caused malignant dysfunction in mesenteric arteries in adolescent SHR offspring

Yuan Zhong1,2, Xueqin Feng1, Ting Xu1

  • 1Institute for Fetology, First Hospital of Soochow University, Suzhou, Jiangsu, China.

Plos One
|April 25, 2019
PubMed

Insights

Prenatal hypoxia in rats led to adolescent hypertension and impaired blood vessel function. This condition was linked to reduced nitric oxide and increased vascular constriction, impacting offspring cardiovascular health.

Area of Science:

  • Cardiovascular Physiology
  • Developmental Biology
  • Hypertension Research

Background:

  • Prenatal hypoxia is a known risk factor for cardiovascular diseases in offspring.
  • Spontaneous hypertension rat (SHR) offspring are predisposed to hypertension.
  • The specific mechanisms linking prenatal hypoxia to adolescent hypertension in SHR are not fully understood.

Purpose of the Study:

  • To investigate if and how prenatal hypoxia causes malignant hypertension and impaired vascular function in adolescent SHR offspring.
  • To elucidate the molecular and cellular pathways involved in hypoxia-induced vascular dysfunction.

Main Methods:

  • Pregnant SHR were exposed to hypoxia (11% O2) or normoxia (21% O2) from gestational day 6 to birth.
  • Offspring body weight and blood pressure were monitored weekly from 5 weeks of age.
  • Mesenteric arteries were analyzed for vascular responses, nitric oxide levels, eNOS expression, and signaling pathways (Ca2+ channels, RhoA/Rock).

Main Results:

  • Prenatal hypoxia caused growth restriction and elevated systolic blood pressure in adolescent SHR offspring.
  • Endothelial-dependent vasodilation was impaired, with reduced responses to acetylcholine and sodium nitroprusside.
  • Decreased plasma nitric oxide and eNOS expression were observed.
  • Enhanced vasoconstriction to phenylephrine was associated with increased L-type calcium channel activity, RhoA/Rock pathway signaling, and intracellular calcium.
  • Vessels exhibited altered mechanical properties (increased stiffness) and structural disorganization.

Conclusions:

  • Prenatal hypoxia significantly affects blood pressure and vascular function in young SHR offspring.
  • Hypoxia-induced hypertension involves impaired endothelial function, reduced nitric oxide bioavailability, and altered vascular smooth muscle contractility.
  • These findings provide insights into the development of hypertension in adolescent offspring with a genetic predisposition.

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