PubMed Health⌕ Search

Biomedical subjects

Mattias Aurell

Publications and source records attributed to Mattias Aurell.

12 recordsLinked to original sources
PubMed2005

Failure of angiotensin II to suppress plasma renin activity in normotensive subjects with a positive family history of hypertension.

The renin-angiotensin system is implicated in the pathophysiology of hypertension. Renin release is regulated by a number of factors, including circulating Ang II (angiotensin II), the so-called short feedback loop. The aim of the present study was to investigate the responsiveness of circulating Ang II on PRA (plasma renin activity) in normotensive subjects with a PFH or NFH (positive or negative family history of hypertension respectively). PRA, renal haemodynamics and urinary sodium excretion were measured during infusion of Ang II without and with pretreatment with the AT1 (Ang II type 1) receptor blocker irbesartan. Normotensive men with a PFH (n=13) and NFH (n=10), with a mean age of 38 years, were given on different occasions intravenous Ang II infusions of 0.1, 0.5 and 1.0 ng.kg-1 of body weight.min-1 before and after pretreatment with 150 mg of irbesartan once a day for 5 consecutive days. RPF (renal plasma flow) and GFR (glomerular filtration rate) were also measured. Before Ang II infusion, the PFH and NFH groups did not differ with respect to BP (blood pressure), body mass index, PRA, RBF (renal blood flow) or urinary sodium. There was no difference in BP or renal haemodynamic response to the highest Ang II dose between the groups. PRA declined with the highest Ang II dose (P<0.01) in subjects with a NFH, but not in subjects with a PFH. After treatment with irbesartan when Ang II had no effect on BP in either group, Ang II also suppressed PRA in subjects with a PFH (P<0.01), and the difference between the groups at baseline was thus eliminated. In conclusion, these findings indicate that subjects with a PFH have a defective Ang II suppression of PRA, which is corrected by AT1 receptor blockade.

Adult↗
PubMed2004

[Adverse effects of lithium treatment and safety routines].

Successful lithium treatment of manic disorders was reported in 1949 by John Cade. This marked the beginning of the pharmacological era in psychiatry. In spite of the emergence of alternative drugs with antimanic and moodstabilising properties, lithium remains the primary long-term treatment for preventing relapse of bipolar disorders. Among the adverse effects of lithium treatment are unintentional lithium intoxication, nephropathy, hypothyroidism, hypercalcemia, hyperparathyroidism, diarrhoea, tremor, weight gain, and effects on the fetus and the newborn child. Early detection or prevention of adverse effects, particularly lithium intoxication, is vital for safety. Therefore, P-lithium and P-creatinine are assessed every 4 months (and pre-lithium) while thyroid and parathyroid function, weight, 24 h consumption of liquids (or 24 h urinary output), B-glucose, and blood pressure are assessed annually (and pre-lithium). Urinary concentrating capacity and glomerular filtration rate are always measured after 5 years of lithium treatment, and always when clinically indicated. Patient education and annual reinforcement of his/her knowledge of pertinent aspects of the treatment and of risk factors for lithium intoxication are important aspects for ensuring safety.

Bipolar Disorder↗
PubMed2003

Increased renal vascular sensitivity to angiotensin II in hypertension is due to decreased response to prostaglandins.

OBJECTIVES: An enhanced sensitivity to angiotensin II in the renal circulation has been demonstrated in the pre-hypertensive phase both in the spontaneously hypertensive rat and in man. To further characterize this abnormality and the role of prostanoids, renal haemodynamics in normotensive young men with a positive (PFH) or a negative (NFH) family history of hypertension were studied. METHODS: Renal vascular reactivity was assessed during infusion of angiotensin II with and without inhibition of prostaglandin synthesis. Normotensive men with PFH (n = 13) and with NFH (n = 10) with a mean age of 38 years were given on two different occasions: (i). angiotensin II infusion i.v. (0.1, 0.5 and 1.0 ng/kg per min) and (ii). angiotensin II infusion after inhibition of prostaglandin synthesis with indomethacin (150 mg daily three consecutive days). Glomerular filtration rate (GFR) and renal plasma flow were measured with renal clearances of chromium edetic acid and para-aminohippuric acid. RESULTS: Before angiotensin II challenge, the groups did not differ with respect to blood pressure, body mass index, plasma renin activity, GFR, renal blood flow (RBF) or urinary sodium excretion. There was no significant difference in systolic or diastolic blood pressure response to angiotensin II between the two groups. In PFH, the lowest angiotensin II dose caused a significant decrease in RBF and increase in renal vascular resistance (RVR) from baseline (P < 0.01 for both). In NFH, only the highest angiotensin II dose produced a significant decrease in RBF and increase in RVR (P < 0.01 for both). During inhibition of prostaglandin synthesis, all three angiotensin II doses caused a significant decrease in RBF (P < 0.02) and increase in RVR (P < 0.02) also in NFH. The renal haemodynamic difference between PFH and NFH was thus eliminated. CONCLUSIONS: These findings indicate that young human subjects with a positive family history of hypertension have a defective vasodilator prostaglandin system, which is responsible for increased renal vascular sensitivity to angiotensin II. Enhanced renal vasoconstriction may be an early event leading to the generation of primary hypertension.

Adult↗
PubMed2002

[Salt, renal function and high blood pressure--reflections on a current issue].

The role of salt intake for blood pressure control has been discussed for a long time. A brief review is given of some pertinent physiological facts to explain this relationship and evolutionary aspects of renal function are emphasized. Salt intake is very high in the modern society, often as high as 15 g sodium chloride per 24 hours while 3-6 g may be more than enough to maintain an adequate salt balance. If the kidneys cannot cope with this severe sodium overload, blood pressure will rise. Therefore, the kidneys' ability to excrete sodium is a key factor and the salt excretion capacity is the kidneys' major barostatic function. As barostats, the kidneys control the blood pressure by ultimately determining the sodium excretion. Reducing sodium intake is, however, difficult as more than 50% of the intake is contained in the food we buy such as bread, sausages, canned food, chips and fast-food. Food products should therefore be "salt declared", but information on this aspect is generally lacking. If the population's salt intake could be reduced by 50%, the prevalence of hypertension will be much reduced, perhaps also by as much as 50%. The cost to society for treating hypertension would be reduced accordingly. Salt intake is also an important aspect of the overweight problem among today's youth. Salt and overweight impose great health risks later in life. Preventive measures in this area must be given high priority in future health care work.

Blood Pressure↗