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Published on: January 31, 2019
Hypertension in Prenatally Undernourished Young-Adult Rats Is Maintained by Tonic Reciprocal
Bernardita Cayupe1, Carlos Morgan2, Gustavo Puentes2
1Centro de Investigación Biomédica y Aplicada (CIBAP), Escuela de Medicina, Facultad de Ciencias Médicas, Universidad de Santiago de Chile (USACH), Santiago 9170020, Chile.
Insights
Prenatal malnutrition leads to adult hypertension in rats. This is driven by overactive connections between the paraventricular nucleus (PVN) and locus coeruleus (LC), involving alpha-1 adrenoceptors and CRH.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Developmental Biology
Background:
- Prenatal malnutrition is a risk factor for adult hypertension.
- Increased alpha-1 adrenoceptor activity in the paraventricular nucleus (PVN) contributes to this hypertension.
- The role of locus coeruleus (LC) to PVN pathways in this condition is unclear.
Purpose of the Study:
- To investigate the contribution of reciprocal excitatory pathways between the locus coeruleus (LC) and paraventricular nucleus (PVN) to prenatal undernutrition-induced hypertension.
- To determine the involvement of alpha-1 adrenoceptor and CRH receptor signaling in these pathways.
Main Methods:
- Microinjection of alpha-1 adrenoceptor and CRH receptor agonists/antagonists into the PVN and LC of rats.
- Measurement of systolic blood pressure and heart rate.
- Assessment of alpha-1 adrenoceptor density and alpha-1A adrenoceptor mRNA expression in relevant brain regions.
Main Results:
- Alpha-1 adrenoceptor and CRH receptor activation increased blood pressure and heart rate in control rats but not in malnourished rats.
- Antagonists reduced hypertension and tachycardia in malnourished rats, with effects reversed by agonists in the complementary nucleus.
- Prenatal undernutrition reduced alpha-1A adrenoceptor mRNA expression in the PVN but did not alter overall hypothalamic alpha-1 adrenoceptor density.
Conclusions:
- Reciprocal excitatory interactions between the PVN and LC, mediated by alpha-1 adrenoceptors and CRH, contribute significantly to hypertension in young adult rats exposed to prenatal malnutrition.
- Altered expression of alpha-1A adrenoceptor in the PVN is a key neurobiological adaptation to early undernutrition, impacting cardiovascular regulation.
Abstract:
Prenatally malnourished rats develop hypertension in adulthood, in part through increased α1-adrenoceptor-mediated outflow from the paraventricular nucleus (PVN) to the sympathetic system. We studied whether both α1-adrenoceptor-mediated noradrenergic excitatory pathways from the locus coeruleus (LC) to the PVN and their reciprocal excitatory CRFergic connections contribute to prenatal undernutrition-induced hypertension. For that purpose, we microinjected either α1-adrenoceptor or CRH receptor agonists and/or antagonists in the PVN or the LC, respectively. We also determined the α1-adrenoceptor density in whole hypothalamus and the expression levels of α1A-adrenoceptor mRNA in the PVN. The results showed that: (i) agonists microinjection increased systolic blood pressure and heart rate in normotensive eutrophic rats, but not in prenatally malnourished subjects; (ii) antagonists microinjection reduced hypertension and tachycardia in undernourished rats, but not in eutrophic controls; (iii) in undernourished animals, antagonist administration to one nuclei allowed the agonists recover full efficacy in the complementary nucleus, inducing hypertension and tachycardia; (iv) early undernutrition did not modify the number of α1-adrenoceptor binding sites in hypothalamus, but reduced the number of cells expressing α1A-adrenoceptor mRNA in the PVN. These results support the hypothesis that systolic pressure and heart rate are increased by tonic reciprocal paraventricular-coerulear excitatory interactions in prenatally undernourished young-adult rats.
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