ABSTRACT
A study was made of all 587 new patients attending an accident and emergency department in the East End of London during one week. Two hundred and twenty-six (39%) cases were not accidents or emergencies; of these, 67% were self-referrals who had not previously seen their general practitioner (GP) and 21% were self-referrals who had previously seen their GP. The four main reasons that these self-referred patients had for attending were that they thought their condition needed immediate attention; they were insufficiently organized to see their GP; they were not registered with a GP; or they wanted a second opinion. Twenty-eight (12%) of the cases which were not accidents or emergencies were referred by a GP. Sixty-nine (12%) of all cases were not registered with a GP. The frequency of cases who were not accidents or emergencies was significantly higher in those not registered than in those registered (0.01 greater than P greater than 0.001). Nineteen (3%) patients were living rough or in hostels. Little abuse of the ambulance service was found.
Subject(s)
Emergency Service, Hospital/statistics & numerical data , Accidents , Adolescent , Adult , Aged , Family Practice , Female , Health Services Misuse , Humans , London , Male , Middle Aged , Referral and ConsultationSubject(s)
Extracellular Space/physiology , Hydrostatic Pressure , Manometry/methods , Pressure , Animals , Humans , Manometry/instrumentation , Models, Biological , Osmotic Pressure , RatsABSTRACT
The role of the kidney in hypertension is reviewed in terms of sodium and water homeostasis, of the secretion of renin inappropriate to the state of sodium and water balance and of other renal humoral factors which might be implicated in the hypertensive process. Fundamental to the long-term maintenance of hypertension is an alteration in the relationship between renal perfusion pressure and the excretion of sodium and water. This alteration may be brought about as a result of renal structural damage, sympathetically mediated renal vasoconstriction or the action of renal or extrarenal hormones which modulate sodium and water excretion. When renin is secreted in excess of the prevailing level of sodium and water balance, the generated angiotensin contributes to the hypertension directly through peripheral and renal vasoconstriction. The level of blood pressure in two hypertensive patients with chronic renal failure was found to be highly correlated with the level of plasma renin activity as this was lowered by the administration of a beta-blocking drug. In rats deprived of sodium, renal artery constriction and contralateral nephrectomy was followed by hypertension without any elevation of plasma angiotensin and with a minimal expansion of plasma volume unaccompanied by expansion of extracellular fluid volume. The possible role of this small volume change and of other possible factors in producing hypertension is discussed. Studies in the nephrectomised rat confirmed eariler reports that renal medullayr auto-explants inhibited renoprival hypertension, but neither the identity nor mode of action of the medullary hypotensive factor were further clarified.
Subject(s)
Diuresis , Hypertension/etiology , Kidney/physiopathology , Water-Electrolyte Imbalance/complications , Angiotensin II/blood , Animals , Blood Pressure , Humans , Hypertension/physiopathology , Natriuresis , Rats , Renin/blood , Water-Electrolyte Imbalance/physiopathologySubject(s)
Blood Pressure , Connective Tissue Cells , Connective Tissue/physiology , Extracellular Space/physiology , Hypertension/etiology , Plasma Volume , Animals , Arginine Vasopressin/pharmacology , Compliance , Extracellular Space/drug effects , Nephrectomy , Osmotic Pressure , Plasma Volume/drug effects , Rats , Renal Artery Obstruction/physiopathologyABSTRACT
"Overloading" with salt and water, i.e., increasing extracellular fluid, can, if maintained for a period, lead to hypertension in which the main hemodynamic abnormality is increased peripheral resistance. There is evidence that salt and water overload is the chief factor in the hypertension of the majority of patients suffering from chronic renal failure. "Overloading" occurs not only when the contents of a container are increased, but also when the capacity of a container is decreased. Reduction of the compliance of the interstitial space would reduce its capacity to hold fluid without increase in pressure. Evidence is presented that the presence of the kidney affects interstitial space compliance; bilateral nephrectomy decreases interstitial space compliance four fold. Hypertension induced by renal artery partial constriction and removal of the other kidney is also associated with reduction of interstitial space compliance; a sudden rise in interstitial space compliance may be the primary factor in the course of events that leads to the rapid fall in blood pressure which occurs when the constriction is removed from the renal artery. It is suggested that the kidney secretes a hormone which increases interstitial space compliance and that this represents a physiological mechanism which enables animals to store water in the interstitial space without undue rise in interstitial tissue pressure. The role of this mechanism in hypertension and in chronic renal failure is discussed.
