During fetal life, gas exchange is carried out in the placenta. The lung does not have a physiological role, apart from possible metabolic functions which include secretion of hormones, enzymatic conversion of inactive substances to functional hormones, and degradation of active materials to inactive metabolites. Blood flow through the lungs is quite low during fetal life; most of the systemic and umbilical venous blood returning to the heart is shunted through the foramen ovale to the left atrium and left ventricle, or through the ductus arteriosus directly from the pulmonary trunk to the descending aorta. About 85-90% of the blood ejected by the right ventricle is diverted from the lungs through the ductus arteriosus (48). Because the right ventri­ cle ejects about 66% of the combined ventricular output of the fetal heart, about 60% of the total output of the heart passes through the ductus arteriosus and thus does not enter the lungs. Should this volume of blood pass through the pulmonary circulation and return to the left ventricle, there would be an unnecessary increase in the volume of work placed on the heart. The low fetal pulmonary blood flow has been explained on the basis of a high pulmonary vascular resistance. Mter birth, however, a marked in­ crease in pulmonary blood flow is necessary to permit adequate gas ex­ change. This review considers: (0) pulmonary arterial pressures and flows in utero and changes during gestation; (b) patterns of fetal pulmonary blood flow; (c) factors that influence fetal pulmonary vascular responses; and (d) mechanisms responsible for the postnatal decrease in pulmonary vascular resistance.

Fetal and Neonatal Pulmonary Circulation

The high sodium-low potassium environment of civilized people, operating on a genetic substrate of susceptibility, is the cardinal factor in the genesis and perpetuation of "essential" hypertension. The noxious effects begin in childhood, when habits of excess salt consumption are acquired at the family table, and are perpetuated by continuing habit and by increasing use of convenience and snack foods with artificially high concentrations of sodium and low levels of potassium. Present methods of food preparation leach out the protective potassium. Extradietary sodium chloride is a condiment not a requirement. Some primitive populations clearly preferred potassium chloride to sodium chloride. Chronic expansion of extracellular fluid volume induced by excess salt consumption causes the central and peripheral circulatory regulatory mechanisms to work at cross purposes, resulting in increased arterial pressure. The protective effect of potassium is dramatic and easily demonstrable in animals and man but its mechanism is not known. It cannot be entirely a direct effect on blood pressure because rats protected with extra potassium against a moderately high salt intake live much longer than control rats but have the same elevated blood pressures. In hypertension with a demonstrable "cause," the high sodium-low potassium environment makes a bad matter worse. In nature, feral man and his forebears were not confronted with excessive sodium and deficient potassium; indeed, the reverse was the case. Evolution has provided powerful mechanisms for conserving sodium and eliminating potassium, but no efficient physiologic mechanisms for conserving potassium and eliminating excess sodium. Most laboratory animal "control" diets contain an amount of sodium that fully suppresses aldosterone secretion, and the same is true of the "average" diet of the American people. Inadequate attention to dietary sodium and potassium makes many studies in both animals and man of uncertain validity. Internally, essential hypertension is an exceedingly complex mosaic of physiologic interactions. Viewed from outside, it is a disorder for which genetic material sets the stage; excessive sodium precipitates it and perpetuates it. Extra salt makes all forms more rapidly progressive and accelerates the onset of terminal events; extra potassium is everywhere protective. When an entire population eats excessively of salt, hypertension will develop among those genetically susceptible, but epidemiologic studies of salt versus blood pressure will not show a relation of salt to hypertension. This is the saturation effect. Low sodium diets are therapeutically effective but generally regarded as an impossible or an unnecessary nuisance. Effective prevention programs must be instituted at as early an age as possible. The efficacy of a prophylactic/therapeutic low sodium-high potassium diet should be weighed against the uncertain hazards of a lifetime of pill taking.

High sodium-low potassium environment and hypertension.

Current State and Future Developments of Noninvasive Treatment of Human Urinary Stones With Extracorporeal Shock Wave Lithotripsy

Estimated Blood Loss and Transfusion Rates Associated with Percutaneous Nephrolithotomy

Keywords: Hypertension, Cardiovascular disease, Diabetes mellitus, Angiotensin II antagonists, ACE inhibitors, Stroke, Heart failure, Post myocardial infarction, Diabetic nephropathy Abstract More than a century of research on the renin- angiotensin system (RAS) has uncovered the widespread involvement of angiotensin II (Ang II) in the pathophysiology of cardiovascular diseases. A number of outcomes-based mega trials utilising hard clinical endpoints have revealed beneficial effects of angiotensin receptor antagonists (AIIAs/ARBs) in patients with hypertension, heart failure, diabetic nephropathy, and post-myocardial infarction (MI). The results of these studies not only emphasise the importance of Ang II in the pathophysiology of these diseases but have provided the basis for an evidence-based approach for the use of AIIAs in clinical practice. It is hoped that the next 100 years of research into the RAS will uncover hitherto unimaginable therapeutic opportunities.

https://journals.sagepub.com/doi/pdf/10.3317/jraas.2006.003

Role of angiotensin II in cardiovascular disease therapeutic implications of more than a century of research.

Monotherapy of Staghorn Renal Calculi: A Comparative Study Between Percutaneous Nephrolithotomy and Extracorporeal Shock Wave Lithotripsy

Extract: This study was designed to investigate the renin-angiotensin system in the fetal lamb Simultaneous measurements of plasma renin activity (PRA) were carried out in seven acute fetal-maternal sheep preparations at 91, 100, 104, 112, 124, 142, and 145 days of gestational age, respectively (term 145 days) The mean fetal PRA in this group was 487 mμ/ml as compared with 158 mμ/ml for the maternal plasma PRA was also measured simultaneously in three intrauterine nonstressed fetuses Six days after insertion of catheters, the fetal PRA was 90, 92, and 875 mμ/ml, respectively, and the maternal PRA was 04, 45, and 375 mμ/ml, respectively The fetal response to aortic constriction was studied in three fetuses and the PRA increased from control values of 48, 55, and 222 mμ/ml to 80, 115, and 345 mμ/ml, respectively, within 15 min after initiation of the aortic constriction and continued to rise to maximum levels of 118, 255, and 380 mμ/ml, respectively PRA then decreased after release to near control levels The maternal PRA did not change significantly during the study period PRA was also measured in the in utero fetus after decreasing the blood volume 8–10% by acute controlled bleeding, and the PRA rose from control values of 60 and 42 mμ/ml to 400 and 544 mμ/ml within 15 min after blood loss, followed by a return towards control values over the subsequent 30 min Morphologic studies in five fetuses, 91–141 days of gestational age, indicate that the juxtaglomerular apparatus contains Bowie-positive smooth muscle granular cells and appears well developed in the fetal kidney by light and electronmicroscopy These studies, therefore, indicate that the renin-angiotensin system is present during fetal development in the sheep and also demonstrate that the fetus does respond to stimuli which, in the adult, result in renin release However, further studies will be necessary in order to establish a definitive physiologic role for renin in the fetus Speculation: The renin-angiotensin system appears to be well developed during fetal development These observations suggest that the enhanced activity of the renin-angiotensin system may play a role in the control of renal hemodynamics and fluid and electrolyte homeostases in the developing fetus

/pdf/the-renin-angiotensin-system-in-the-fetal-lamb-4f4793z42s.pdf

The renin-angiotensin system in the fetal lamb.

Chronic hypertension caused by unilateral constriction of the renal artery in the presence of the opposite untouched kidney can be produced in the dog by progressive plication of the renal artery over a period of several hours. Twenty-three female dogs were studied. Mean arterial blood pressure was measured in the unanesthetized recumbent dog by direct puncture of the femoral artery. Reproducible control blood pressure readings were obtained only after daily training of the animals for at least 2 months. Mean arterial blood pressure for the whole group of animals was 98.25 ± 7.45 (SD) mm Hg prior to constriction. Three months after constriction, the mean arterial blood pressure of the group of dogs with a 50-63% reduction in renal blood flow was 132.4 ± 5.51 (SD) mm Hg (P < 0.001); for the group with a 78-86% reduction in renal blood flow it was 144.68 ± 10.68 (SD) mm Hg (P < 0.001). Six dogs from these two groups underwent ipsilateral nephrectomies 4-16 months after constriction, and their elevated arter...

Andrei N. Lupu

Papers

Monotherapy of Staghorn Renal Calculi: A Comparative Study Between Percutaneous Nephrolithotomy and Extracorporeal Shock Wave Lithotripsy

The renin-angiotensin system in the fetal lamb.

Experimental Unilateral Renal Artery Constriction in the Dog

Carcinoma of deep male urethra.

Treatment of ureteral calculi by extracorporeal shock-wave lithotripsy UCLA experience