Differences between perinatal angiotensin binding in the brains of SHR and WKY rats

Cook, Vickie I.; Grove, Kevin L.; Speth, Robert C.; McMENAMIN, K. M.; Harding, Joseph W.

doi:10.1016/0167-0115(93)90366-g

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…AngII microinjected into the SFO causes a pressor effect that is mediated by vasopressin release and increased sympathetic activity (46,15). Elevated brain AngII binding sites have also been reported in spontaneously hypertensive fetal and newborn rats (47,48), and blockade of central RAS in adult spontaneously hypertensive rat can reverse their chronic hypertension (49). The underlying mechanisms and regulatory processes that lead to increased AT 1 receptor brain expression in 9% offspring are unknown but may involve a defect in nitric oxide pathway (27,50,51), positive feedback regulation by elevated brain AngII (52,53), and glucocorticoids (12,54,55).…”

Section: Table 2 Spectral Measurements Of Arterial Bpv In 9-to 12-wkmentioning

confidence: 93%

Role of Brain and Peripheral Angiotensin II in Hypertension and Altered Arterial Baroreflex Programmed during Fetal Life in Rat

et al. 2004

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Intrauterine programming of hypertension is associated with evidence of increased renin-angiotensin system (RAS) activity. The current study was undertaken to investigate whether arterial baroreflex and blood pressure variability are altered in a model of in utero programming of hypertension secondary to isocaloric protein deprivation and whether activation of the RAS plays a role in this alteration. Pregnant Wistar rats were fed a normalprotein (18%) or low-protein (9%) diet during gestation, which had no effect on litter size, birth weight, or pup survival. Mean arterial blood pressure (MABP; 126 Ϯ 3 mm Hg 9% versus 108 Ϯ 4 mm Hg 18%; p Ͻ 0.05) and blood pressure variability were significantly greater in the adult offspring of the 9% protein-fed mothers. Arterial baroreflex control of heart rate, generated by graded i.v. infusion of phenylephrine and nitroprusside, was significantly shifted toward higher pressure; i.v. angiotensinconverting enzyme inhibitor normalized MABP and shifted the arterial baroreflex curve of the 9% offspring toward lower pressure without affecting the 18% offspring. For examining whether brain RAS is also involved in programming of hypertension, angiotensin-converting enzyme inhibitor and losartan (specific AT 1 receptor antagonist) were administered intracerebroventricularly; both significantly reduced MABP of the 9% but not the 18% offspring. Autoradiographic receptor binding studies demonstrated an increase in brain AT 1 expression in the subfornical organ and the vascular organ of the lamina terminalis in the 9% offspring. These data demonstrate a major tonic role of brain and peripheral RAS on hypertension associated with antenatal nutrient deprivation. Abbreviations ACE-I, angiotensin-converting enzyme inhibitor AngII, angiotensin II AP, area postrema BPV, blood pressure variability HR, heart rate ICV, intracerebroventricular MABP, mean arterial blood pressure MEPO, median preoptic nucleus NTS, nucleus of the solitary tract OVLT, vascular organ of the lamina terminalis PVH, paraventricular nucleus of the hypothalamus RAS, renin-angiotensin system SFO, subfornical organ Chronic cardiovascular diseases of adults can have their origins in fetal life. Epidemiologic studies reveal that hypertension, stroke, and coronary heart disease are inversely related to birth weight (1) and that this relationship is independent of genetic factors (2) and lifestyle (3). It has been suggested that a poor nutrient supply at a critical period of early development leads to permanent alterations in the programming of the developing cardiovascular structures or functions (4). This concept has been supported by animal studies demonstrating an association between nutritional deficit during fetal life and increased blood pressure in adulthood (5, 6).Experimental evidence suggests that activation of the reninangiotensin system (RAS) (7,8) is an important element of hypertension programmed during fetal life. Infants who are born with intrauterine growth restriction have increased plasma renin activity and r...

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Section: Table 2 Spectral Measurements Of Arterial Bpv In 9-to 12-wkmentioning

confidence: 93%

Role of Brain and Peripheral Angiotensin II in Hypertension and Altered Arterial Baroreflex Programmed during Fetal Life in Rat

et al. 2004

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“…With the knowledge that RAS components appear early in development, and have an association with cellular growth, it is not unlikely that an irregularity occurring during neurogenesis could contribute to abnormalities of developmental as well as subsequent diseases such as hypertension (Cook et al, 1993). In fetal tissues, AT2 receptors are abundantly and widely expressed, but in the adult, they are present only in restricted tissues such as in the atretic ovary.…”

Section: Functional Development Of the Fetal Brain Rasmentioning

confidence: 99%

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Mao

Shi

et al. 2009

Progress in Neurobiology

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Since the concept of fetal origins of adult diseases was introduced in 1980s, the development of the renin-angiotensin system (RAS) in normal and abnormal patterns has attracted attention. Recent studies have shown the importance of the fetal RAS in both prenatal and postnatal development. This review focuses on the functional development of the fetal brain RAS, and ontogeny of local brain RAS components in utero. The central RAS plays an important role in the control of fetal cardiovascular responses, body fluid balance, and neuroendocrine regulation. Recent progress has been made in demonstrating that altered fetal RAS development as a consequence of environmental insults may impact on "programming" of hypertension later in life. Given that the central RAS is of equal importance to the peripheral RAS in cardiovascular regulation, studies on the fetal brain RAS development in normal and abnormal patterns could shed light on "programming" mechanisms of adult cardiovascular diseases in fetal origins.

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Fosinopril treatment of pregnant rats: developmental toxicity, fetal angiotensin-converting enzyme inhibition, and fetal angiotensin II receptor regulation

et al. 1995

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Differences between perinatal angiotensin binding in the brains of SHR and WKY rats

Cited by 4 publications

References 32 publications

Role of Brain and Peripheral Angiotensin II in Hypertension and Altered Arterial Baroreflex Programmed during Fetal Life in Rat

Role of Brain and Peripheral Angiotensin II in Hypertension and Altered Arterial Baroreflex Programmed during Fetal Life in Rat

Development of fetal brain renin–angiotensin system and hypertension programmed in fetal origins

Fosinopril treatment of pregnant rats: developmental toxicity, fetal angiotensin-converting enzyme inhibition, and fetal angiotensin II receptor regulation

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