Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Onset of paralysis by cervical spinal cord injury led immediately to temporary adrenocortical activation and, within 2 days, to sustained skin and bone breakdown. Urine cAMP was increased, blood parathyroid hormone, renin activity, and electrolytes were normal, and fluid and electrolytes balance became negative during the initial 6 days of paralysis.
Paraplegia 1977 Nov
PMID:Immediate endocrine and metabolic consequences of traumatic quadriplegia in a young woman. 20 1

It is now recognized that orthostatic hypotension occurs as a complication of many neurological diseases. An account is given of some of those in which it may develop. The pathological lesions frequently allow studies to be made of physiological mechanisms remaining in the isolated parts of the nervous system. For example transection of the cervical spinal cord causes complete separation of peripheral sympathetic pathways from the control of the brain. It was possible, therefore, to examine the control of renin release and also cerebral blood flow regulation during change of blood pressure in patients with some of these disorders. Evidence has been obtained that the renin-angiotensin system is active in paraplegia and in many other patients with orthostatic hypotension. In addition symptoms of cerebrovascular insufficiency are minimized by the retention of autoregulation of cerebral blood flow (CBF) in patients with failure of sympathetic function. Autoregulation maintains CBF within wide limits of blood pressure and symptoms of orthostatic hypotension only develop if the blood pressure falls below the lower limit, usually about 70 mm Hg.
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PMID:Orthostatic hypotension in neurological disease. 78 5

The metabolic effects of sodium restriction, alone or with thiazide, were studied in 12 healthy subjects, in 24 tetraplegics during the intial 8 months of paralysis (early) and in 16 others during the subsequent period (late). The diuresis caused by both treatments led to more haemoconcentration in early than in late patients. In contrast with the healthy subjects on low sodium, the tetraplegics had a delayed urinary sodium retention and no fall in calciuria. During thiazide, urinary sodium depletion occurred early and the urine calcium fell after 3 days in all tetraplegics. During both treatments, aldosterone and renin increased more in early patients than in the other groups. The clinical implications of inducing dehydration and a sustained stimulation of the renin-angiotensin-aldosterone axis in recently injured tetraplegics with severe orthostatic hypotension are discussed.
Paraplegia 1977 May
PMID:Metabolic effects of sodium restriction and thiazides in tetraplegic patients. 89 54

Many patients with high spinal cord injury experience exaggerated blood pressure rises in response to bladder distension. To examine the humoral mechanisms associated with these responses, ECG heart rate, blood pressure and vasoactive hormone levels were measured at baseline and during bladder distension following slow bladder filling in 23 subjects: 9 high spinal lesion patients, 7 low spinal lesion patients and 7 normal control subjects. Systolic blood pressure rose significantly during bladder distension in the high spinal lesion group by an average of 56 mm Hg (48%) and diastolic blood pressure rose by 22 mm Hg (47%), while heart rate fell by a mean of 7.4 beats per minute (15%). By contrast, neither systolic or diastolic blood pressure nor heart rate changed significantly during bladder distension in the low spinal lesion or normal control group. There were no significant changes in plasma levels of noradrenaline, renin, aldosterone, vasopressin, arginine, or atrial natriuretic peptide during bladder distension to account for the blood pressure rise in the high spinal lesion group. These findings suggest that humoral mechanisms are unlikely to play a major role in the mediation of pressor responses to bladder distension in high spinal lesion patients.
Paraplegia 1992 May
PMID:Cardiovascular and vasoactive hormone responses to bladder distension in spinal and normal man. 159 76

One to two per cent of children and up to 11% of adolescent have arterial hypertension. In most cases children and adolescent are not recognized to be hypertensive because physicians do not routinely measure blood pressure. Often the diagnosis is recognized only when the pediatric patients develop a complication: seizure, stroke, heart failure or paraplegia. Renovascular hypertension in children and adolescents is more common than all of the other causes combined, except for coarctation of the aorta. The diagnosis is not so easy and includes the usual history, physical examination (signs and symptoms of coarctation of the isthmic or abdominal aorta or of an abdominal mass or of one of the adrenal causes of hypertension), laboratory studies, abdominal ultrasound study and chest x-ray. Sometime a CAT can be usefull. The next steps are the early and rapid-sequence IVP, renal angiography and peripheral and renal renin activity. The management of renovascular hypertension in children and adolescent includes a conservative approach (percutaneous transluminal renal angioplasty or renal embolization), rarely used in pediatric age, and the surgical treatment. This latter includes all the surgical procedures of renal revascularization and, in unilateral renal parenchymal diseases, the nephrectomy or a partial nephrectomy. The postoperative results are very good in a high percentage of cases. In bilateral cases, the revascularization surgical procedures improve or normalize also the impaired renal function.
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PMID:[Renovascular hypertension in childhood]. 182 81

The development of persistent hypertension in young, previously healthy paraplegic individuals is unusual; it could be postulated that hypertension is a cardiovascular response peculiar to patients who sustained spinal cord injury after surgical repair of the aorta with trauma-related injuries. In a retrospective study of 712 patients sustaining spinal cord injury during the last decade, seven sustained paraplegia after aortic repair that was necessitated by trauma-related injuries. Despite the low incidence of new-onset hypertension in paraplegic patients, five of the seven developed hypertension, of which three required chronic antihypertensive medications. It is well documented that patients with lesions of the neuraxis above the sixth thoracic segment are prone to the phenomenon of autonomic hyperreflexia. This results from interruption of the baroreceptor reflex and the descending tracts of the spinal cord. There is evidence that the renin-angiotensin system, catecholamines, and receptor-site activity play an important role in the control of blood pressure in spinal cord injured patients. Additional investigation of this rare subgroup of spinal cord injured patients may further illuminate the effect of spinal cord injury on autonomic control of the cardiovascular system.
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PMID:Persistent hypertension in young spinal cord injured individuals resulting from aortic repair. 192 98

We have studied the haemodynamic, hormonal and urinary effects of postural change in 6 tetraplegic patients, 6 paraplegic patients and 6 normal subjects. Measurements of blood pressure and heart rate, plasma renin activity, plasma aldosterone, urine volume and electrolyte excretion were made for 60 minutes while sitting and 60 minutes while recumbent. In tetraplegics the blood pressure was lower when sitting and rose during recumbency, unlike paraplegics and normal subjects. Plasma renin activity and aldosterone were higher in tetraplegics when sitting compared to normal subjects and did not fall during recumbency. Urine output increased significantly after recumbency in tetraplegics, but not in paraplegics or normal subjects. Both urinary sodium and potassium excretion were lower in tetraplegics and higher in paraplegics compared to normal subjects when sitting. In paraplegics the fall in both sodium and potassium excretion did not appear to be related to change in posture. Our observations indicate that recumbency induces a diuresis in tetraplegics but not in paraplegics or in normal subjects. The diuresis in tetraplegics may be related to the accompanying haemodynamic and hormonal changes induced by recumbency.
Paraplegia 1988 Aug
PMID:Haemodynamic, hormonal and urinary responses to postural change in tetraplegic and paraplegic man. 305 Jul 96

Nineteen mongrel dogs had 30 minutes of thoracic aortic occlusion to determine the effects that blockade of the renin-angiotensin system may have on preserving spinal cord blood flow and function during a period of temporary spinal cord ischemia. Cross-clamping of the thoracic aorta causes renal ischemia and activates the renin-angiotensin system with resulting increased production of angiotensin II. Angiotensin II is a potent peripheral constrictor and elevated levels may constrict collateral spinal cord circulation. At the time of aortic cross-clamping, 10 dogs received 100 mg/kg of MK422 (intravenous enalapril maleate), a converting enzyme inhibitor, and nine animals served as controls. The blockade of the renin-angiotensin system had no preserving effects on spinal cord flow as measured by microspheres and on spinal cord function as graded with the Tarlov scale. However, the paraplegic animals all had significantly increased lower thoracic and lumbar spinal cord flows 30 minutes after clamp release when compared with those animals that remained neurologically intact. In conclusion, marked hyperemia occurring after a period of hypoperfusion may lead to spinal cord edema and compartment syndrome with resulting paraplegia.
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PMID:The effect of hyperemia on spinal cord function after temporary thoracic aortic occlusion. 317 89

This paper has reviewed the acute and long-term responses to changes in vertical posture in normal and tetraplegic subjects. It has discussed physiological mechanisms causing orthostatic hypotension in acute cervical spinal cord injured patients, and subsequent factors contributing to its amelioration over time. The long-term adaptive mechanisms are still controversial, probably involving multiple neurological, endocrine, renal, cardiovascular and haemodynamic factors. These factors include inhibition of vagal tone, plasma catecholamine levels, sensitivity of vascular beds to catecholamines, stretch reflexes in blood vessels, spinal BP reflexes, renin-angiotensin system, aldosterone and plasma volume changes. Individual differences may also interact with these various mechanisms, further complicating the issues. Although the fact that most tetraplegics do improve their orthostatic tolerance over time with repeated tilting is manifest, the precise mechanisms allowing this improvement are not. Research is needed to clarify these adaptive mechanisms, as well as to investigate the physiological effects of long-term therapeutic standing in devices such as standing frames.
Paraplegia 1984 Apr
PMID:Cardiovascular and haemodynamic responses to tilting and to standing in tetraplegic patients: a review. 637 66

We present the case of a 60 year old C6 complete tetraplegic patient who developed profound hypotension following initiation of the angiotensin-converting enzyme inhibitor lisinopril to control blood pressure. Other causes of hypotension, such as myocardial infarction and sepsis was ruled out. Inhibition of the renin-angiotensin-aldosterone system was the probable cause of hypotension. This case demonstrates the critical importance of the renin-angiotensin-aldosterone axis in the maintenance of blood pressure in tetraplegic patients, who may lack input from the brain to sympathetic neurons, and therefore have increased reliance on the renin-angiotensin-aldosterone axis for the maintenance of blood pressure. Angiotensin-converting enzyme inhibitors should be avoided in tetraplegic patients, unless other treatment modalities are ineffective.
Paraplegia 1994 Dec
PMID:Profound hypotension in a tetraplegic patient following angiotensin-converting enzyme inhibitor lisinopril. Case report. 770 26


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