Aetiology of Hypertension

Abstract

We are still uncertain of the way in which environment and heredity interact to produce increased arterial pressure in patients with essential hypertension. Few indisputable abnormalities can be demonstrated. Of these there is universal agreement that structural vessel hypertrophy is present and this acts probably as a maintenance and perhaps amplifying system resulting from an initial increase in arterial pressure. It cannot of course explain an increase in arterial pressure ab initio. Most of the well defined systems of arterial pressure control do not show any marked abnormality, although there is some evidence for a modest degree of sympathetic nervous system overactivity. Although some of the changes in cation fluxes across erythrocyte and leucocyte membranes are still debatable, there is general agreement that cation handling by erythrocytes and leucocytes is abnormal in many patients with essential hypertension and that some of these abnormalities are shared by the normotensive relatives of hypertensive patients. The most promising approach is that there is an abnormality of the cell membrane vascular smooth muscle which is partly genetically determined and perhaps also involves the autonomic nervous system. This produces an increased pressor response to environmental stimuli which becomes perpetuated and perhaps amplified by structural hypertrophy of the resistance vessels.

Non-invasive Blood Pressure Measurements in Cats: Clinical Significance of Hypertension Associated with Chronic Renal Failure.

“…Renal parenchymal disease, renovasucular disease, diabetes, Cushing's syndrome, primary aldosteronism, pheochromocytoma and hypothyroidism have all been cited as main causes of secondary hypertension. Hypertension with renal disease (renal hypertension) occurs with the highest frequency [6,9,17]. On the other hand, hypertension is related to impaired renal function in cats, although there has been little research into feline hypertension [7,8,11,16].…”

“…Thus, there has been very little research on hypertension in the field of veterinary medicine. Hypertension per se progresses without displaying any specific clinical symptoms, and there is difficulty in measuring the blood pressure in awake animals.Hypertension consists of essential and secondary hypertension, and the most common cause of secondary hypertension is considered to be renal parenchymatous disease [6,9,15,17]. In our previous work, a correlation between renal disease and hypertension was identified in dogs using the oscillometric method [12].…”

“…Hypertension consists of essential and secondary hypertension, and the most common cause of secondary hypertension is considered to be renal parenchymatous disease [6,9,15,17]. In our previous work, a correlation between renal disease and hypertension was identified in dogs using the oscillometric method [12].…”

A Clinical Evaluation of Blood Pressure through Non-Invasive Measurement Using the Oscillometric Procedure in Conscious Dogs.

“…The causes of secondary hypertension include renal parenchymal disease, renovascular disease, diabetes, Cushing's syndrome, primary aldosteronism, chromaffinoma, hypothyroidism, and the like. Renal disease is the most frequent cause of hypertension [8,9,18]. On the contrary, essential hypertension is said to be extremely rare although there have only been a few studies on canine hypertension [3,11,20].…”

Study of prevalence and impact of hyperuricemia in a patient of hypertension

“…3 Serum uric acid was first noted to be associated with increased BP by Frederick Mohamed in the 1870s. 4 The mechanism(s) by which UA may engender organ damage is still incompletely understood, but there is increasing evidence that endothelial dysfunction is a fundamental mechanism whereby this substance may affect cardiovascular and renal function and structure. 5 The aim of the study was to assess serum uric acid levels in hypertensive patients, to associate changes in serum uric acid with clinical prognosis, to study relation between severity of hypertension to serum uric acid level.…”