Maternal high-salt diets affected pressor responses and microvasoconstriction via PKC/BK channel signaling pathways in rat offspring.
METHODS
High-salt (HS) intake is linked to hypertension, and prenatal exposure to maternal HS diets may have long-term impact on cardiovascular systems. The relationship between HS diets and cardiovascular disease has received extensive attention. This study determined pressor responses and microvessel functions in the adult offspring rats exposed to prenatal HS.


RESULTS
The offspring of 5-month old as young adults in rats were used. Blood pressure, vascular tone, intracellular Ca(2+), and BK channels in mesenteric arteries were measured in the offspring. Phenylephrine (Phe)-induced pressor responses were significantly higher in the prenatal HS offspring. Vessel tension and intracellular Ca(2+) concentrations associated with Phe-induced pressor responses were increased in the mesenteric arteries of the HS offspring. PKC α- and δ-isoforms were upregulated in mesenteric arteries of the HS offspring. The enhanced Phe-mediated vascular activity was linked to the altered PKC-modulated BK channel functions.


CONCLUSIONS
The results suggested that prenatal exposure to HS altered microvascular activity probably via changes in PKC/BK signaling pathways, which may lead to increased risks of hypertension in the offspring.
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Le
L
Bo
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Lin
L
Jiang
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Anwen
A
Zhou
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Chonglong
C
Wu
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Jiayue
J
Li
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Qinqin
Q
Gao
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Pengjie
P
Zhang
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Juanxiu
J
Lv
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Na
N
Li
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Xiuxia
X
Gu
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Zhoufeng
Z
Zhu
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.
Caiping
C
Mao
Institute for Fetology & Reproductive Medicine Center, First Hospital of Soochow University, Suzhou, P. R. China.|Center for Prenatal Biology, Loma Linda University, CA, USA.
Zhice
Z
Xu
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D004032:Diet; D005260:Female; D006973:Hypertension / Q000209:etiology / Q000473:pathology; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000235:genetics* / Q000378:metabolism; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D008638:Mesenteric Arteries / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology; D011247:Pregnancy; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism*; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D015854:Up-Regulation; D014661:Vasoconstriction / Q000187:drug effects*
D051036:Large-Conductance Calcium-Activated Potassium Channels; D017673:Sodium Chloride, Dietary; D010656:Phenylephrine; D011493:Protein Kinase C; D002118:Calcium
Hypertension; Large-conductance Ca2+-activated K+ channels; Prenatal high-salt; Protein kinase C; Vasoconstriction