The Blood Pressure of the Fetal Rat and Its Response to Renin and Angiotonin

Burlingame, Paul L.; Long, J. A.; Ogden, Eric

doi:10.1152/ajplegacy.1942.137.3.473

Cited by 30 publications

(11 citation statements)

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“…The smallest effective doses of adrenaline and noradrenaline in the foetus is weight for weight 20-25 times the minimal effective adult dose; this relative insensitivity of the foetal response to adrenaline was noted previously by Clark (1932) in the cat, and by Burlingame, Long & Ogden (1942) in the rat. The large doses of adrenaline and noradrenaline, when injected intravenously in both rabbit and guinea-pig foetuses, produce changes in the blood pressure resembling those produced by moderate doses in the adult: the rise in the arterial pressure is accompanied by a greater rise in pulse pressure with adrenaline than noradrenaline.…”

Section: Discussionsupporting

confidence: 52%

The action of adrenaline and noradrenaline on the placental and foetal circulations in the rabbit and guinea‐pig

Dornhorst¹,

Young²

1952

The Journal of Physiology

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The original object of the investigation was to find whether the placental barrier was permeable to adrenaline and to noradrenaline. It soon became apparent that whereas the placental vessels were very sensitive to these hormones, the foetus itself was relatively insensitive. These findings will now be described. METHODSThe observations were made on rabbits, 28-31 days pregnant, and guinea-pigs, 40-63 days pregnant. Light anaesthesia was maintained with urethane 1-5 g/kg body weight, injected intravenously. The guinea-pigs were lightly anaesthetized with ether while a vein was exposed for the injection. A maternal jugular vein was cannulated with fine polythene tubing for the infusion or injection of drugs. The maternal arterial blood pressure was recorded with a capacitance manometer from a carotid artery which was also cannulated with fine polythene tubing. The abdominal wall was opened by a mid-line incision under saline at 380 C. The uterus was cut longitudinally from rump to crown of a single foetus and that foetus was then delivered into the saline and supported throughout the experiment on a gauze sling. The foetal arterial blood pressure was recorded with a capacitance manometer from one carotid artery which was cannulated with a no. 19 record needle. Intrafoetal injections were made into the jugular vein or, in the guinea-pig, into the vitelline vein, towards the foetus. RESULTSL-Adrenaline, L-noradrenaline and oxytocin in the maternal circulation A continuous infusion of adrenaline, at the rate of 06 ,ug/kg/min, increased the maternal blood pressure by 10-25 mm Hg (with or without accelerating the heart rate) and caused vigorous contractions of the uterine muscle. The placenta became blue, the foetal heart rate fell from an average value of 300 per min to 150-170 per min, and the foetal blood pressure decreased from

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Section: Discussionsupporting

confidence: 52%

The action of adrenaline and noradrenaline on the placental and foetal circulations in the rabbit and guinea‐pig

Dornhorst¹,

Young²

1952

The Journal of Physiology

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“…2) (25,26). These changes in wall structure are regarded as adaptations to rapidly increasing blood pressure (i.e., rising >50 mm Hg in the first 2 weeks) (27). Aortic remodeling during this period may require many of the same abilities (e.g., migration, proliferation, synthesis of extracellular matrix molecules) needed at earlier stages of development, perhaps including production of PDGF-like molecules.…”

Section: Resultsmentioning

confidence: 99%

Expression and developmental control of platelet-derived growth factor A-chain and B-chain/Sis genes in rat aortic smooth muscle cells.

Majesky

Benditt

Schwartz

1988

Proc. Natl. Acad. Sci. U.S.A.

200

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Cultured arterial smooth muscle cells (SMC) can produce platelet-derived growth factor (PDGF)-like molecules. This property raises the possibility that SMC-derived PDGFs function as autocrine/paracrine regulators in the formation and maintenance of the artery wall. In this study we have asked if levels of mRNAs directing synthesis of PDGF are modulated in aortic SMC during postnatal development. We report here that genes encoding PDGF A-and B-chain precursors are expressed at similar low levels in intact aortas from newborn and adult rats. Marked differences in regulation of transcript abundance of these genes were revealed when aortic SMC were grown in cell culture. PDGF B-chain transcripts accumulated in passaged newborn rat SMC but not adult rat SMC, whereas PDGF A-chain RNA was found in comparable amounts in SMC from both age groups. Similarly, SMC from newborn rats secreted at least 60-fold more PDGF-like activity into conditioned medium than did adult rat SMC. PDGF B-chain transcripts in newborn rat aortic SMC are short-lived and increased 5-fold by 3 hr after treatment with cycloheximide. In contrast, PDGF A-chain transcripts are more stable, and their constitutive levels were generally unaffected by cycloheximide. These results show that PDGF A-and B-chain genes are transcribed in the normal rat aorta and provide evidence for age-related change in the control of PDGF B-chain gene expression in aortic SMC. Independent regulation of transcript levels in cultured SMC leaves open the possibility that PDGFs of different composition (AA, AB, BB) play different roles in normal function of the artery wall.The discovery that arterial smooth muscle cells (SMC) in culture produce peptide growth factors thought to be required for their own growth (1-4) provides new perspectives on control of SMC proliferation in the intact artery wall. Previously, a role for platelet-and inflammatory cell-derived mitogens in initiation of SMC growth has been emphasized (5), particularly for repair of arterial wounds. However, SMC replication in normal development (6), medial thickening in hypertension (7), and certain focal proliferations in the arterial intima (8-10) occur in the absence of thrombosis or inflammatory cell responses. These forms of SMC proliferation might be initiated by growth factors produced within the artery wall itself. Furthermore, SMC migration and replication at sites of arterial injury or advancing atherosclerotic plaques might be enhanced by endogenously produced growth factors acting in concert with those released from platelets and adherent leukocytes.The concept that SMC replication in vivo depends upon growth factors produced within the intact vessel wall is supported by the observations that in vitro both endothelial cells (11, 12) and SMC secrete molecules that structurally and functionally resemble platelet-derived growth factor (PDGF) from human platelets. Seifert et al. (1) showed that aortic SMC from newborn rats released PDGF-like activity into conditioned medium and had greatly reduced ...

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“…The left ventricle, on the other hand, is additionally exposed to a rapidly increasing pressure load. Mean arterial blood pressure in the rat has been measured to be approximately 14 mm Hg at birth (Burlingame et al, 1942), 35 mm Hg at 5 days (Litchfield, 1958), and 52-56 mm Hg during the 2nd postnatal week (Litchfield, 1958;Rakusan et al, 1965). Increasing pressure load in the adult heart induces concentric ventricular hypertrophy, in which wall thickness increases without chamber enlargement (Grant et al, 1965).…”

Section: Discussionmentioning

confidence: 99%

“…All perfusions were done at a pressure of 30 mm Hg, the minimal level at which a reliable flow through the tissue could be attained. This pressure is equal to the average mean arterial pressure measured in anesthetized rats between the ages of birth and 11 days (Burlingame et al, 1942;Litchfield, 1958).…”

Section: Methodsmentioning

confidence: 99%

Morphometric study of early postnatal development in the left and right ventricular myocardium of the rat. I. Hypertrophy, hyperplasia, and binucleation of myocytes.

Anversa¹,

Olivetti²,

Loud³

1980

Circulation Research

185

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SUMMARY We reviewed the absolute amd differential growths of the myocyte populations in the left (L) and right (R) ventricular myocardium morphometrically from 1 to 5 days and from 5 to 11 days after birth. From 1 to 11 days hypertrophy of the average myocyte in the ventricles was (L) 2.7-and (R) 2.4-fold, and myocyte proliferation was (L) 2.0-and (R) 1.2-fold. Mean cell volume, cell length, and percent binucleation of cardiac myocytes were similar in both ventricles at 1, 5, and 11 days of age. During this period, average myocyte length increased 2-fold (12 sarcomere lengths), and the percentage of binucleate myocytes increased approximately from 2.7 to 17 to 48%. Myocyte hypertrophy from 1 to 5 days resulted mainly from an increase in the volume of cytoplasm per nucleus and from 5 to 11 days from the accumulation of binucleate cells. No differences were observed in the characteristics of epicardial and endocardial myocytes in either ventricle up to 11 days of age. The 61% greater proliferation of myocytes in the left ventricle was the principal basis for the development of a 2-fold difference in ventricular weight gains: (L) 6.2-and (R) 3.4-fold. No increase in right ventricular midwall thickness was observed, in contrast to a 2.7-fold increase of the left ventricle. It was concluded that, as a result of the circulatory changes occurring shortly after birth, right ventricular growth is analogous to eccentric hypertrophy, whereas left ventricular growth represents a combination of eccentric and concentric hypertrophy. Circ Res 46: 495-502, 1980 GROWTH of the myocardium during the early postnatal period must accommodate not only the increasing demands of the rapidly growing animal but also the relatively abrupt changes in the patterns of blood flow and circulatory resistance occuring shortly after birth. Work required of the left and right ventricles is approximately equal as they pump in parallel during fetal life (Heymann and Rudolph, 1973;Rudolph, 1974). With closure of the foramen ovale and ductus arteriosus after birth, blood flow is henceforth in series through the right and left ventricles, resulting in a greater volume work load on each ventricle. In the same period, pulmonary resistance is lowered by expansion of the collapsed lungs (Klopfenstein and Rudolph, 1978;Rudolph, 1979), peripheral resistance increases with loss of the placental circulation (Rudolph, 1970), and the pressure load on the left ventricle becomes significantly greater than that on the right ventricle (Assali et al., 1965). The combi-

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The Blood Pressure of the Fetal Rat and Its Response to Renin and Angiotonin

Cited by 30 publications

References 0 publications

The action of adrenaline and noradrenaline on the placental and foetal circulations in the rabbit and guinea‐pig

The action of adrenaline and noradrenaline on the placental and foetal circulations in the rabbit and guinea‐pig

Expression and developmental control of platelet-derived growth factor A-chain and B-chain/Sis genes in rat aortic smooth muscle cells.

Morphometric study of early postnatal development in the left and right ventricular myocardium of the rat. I. Hypertrophy, hyperplasia, and binucleation of myocytes.

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