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Biomedical subjects

G Rinaldi

Publications and source records attributed to G Rinaldi.

At least 55 records · Page 3Linked to original sources
PubMed1988

Plasma membrane and its abnormalities in hypertension.

The plasma membrane is composed of proteins embedded in a discontinuous fashion in a lipid bilayer. These proteins maintain the integrity of the membrane and play fundamental roles as ion transport channels and as receptors for agents that regulate cell function. The membrane is therefore an important regulator of vascular smooth muscle contraction. The plasma membrane in the hypertensive animal exhibits abnormal permeability for monovalent ions and defective calcium handling. This is reflected in fewer calcium-binding sites and, as a result, in deficient membrane stabilization. These defects have been identified in several cell types, including lymphocytes, red blood cells, adipocytes, and vascular smooth muscle cells. Evidence presented in the current review suggests that hypertension is associated with a generalized membrane defect. Abnormalities in ion transport in vascular smooth muscle cells are the most relevant to the pathogenesis of hypertension since they could be directly responsible for the rise in blood pressure. We hypothesize that the impaired stabilizing effect of calcium in vascular smooth muscle cells of hypertensive subjects renders the membrane more excitable and that this in turn leads to increased vascular reactivity and higher peripheral resistance. Peripheral vascular reactivity usually is increased in hypertension, suggesting increased responsiveness of the smooth muscle cells. Possible abnormalities of the several components of the contractile process of these cells have been investigated for the role they might play in this altered response. Abnormalities in the plasma membrane have been most clearly defined and are emphasized in this review.

Animals↗
PubMed1986

[Essential arterial hypertension: main vasodilator effect of nifedipine].

The acute effects of a single dose of nifedipine (NIF, 20 mg SL) on heart rate (HR), arterial pressure (AP), forearm blood flow (FBF) and forearm vascular resistance (FVR), were measured in 15 normotensive (NP) and 11 hypertensive (HP) patients. In NP, NIF increased HR (from 78 +/- 3 to 88 +/- 3 lat/min, P less than 0.05) and FBF (from 4.0 +/- 0.4 to 5.5 +/- 0.3 ml/min. 100 ml, P less than 0.05) and decreased AP (from 99 +/- 2 to 89 +/- 3 mmHg, P less than 0.05) and FVR (from 29 +/- 3 to 22 +/- 2.9 relative units, P less than 0.05). In HP the changes were (with the exception of HR, which did not vary significantly) much greater in magnitude, and directly correlated with pretreatment levels of AP. In vitro experiments in aortic rings from spontaneously hypertensive (SHR) and normotensive (NR) rats demonstrated a much greater sensitivity of SHR to the relaxant effect of NIF, while the relaxant effect of nitroglycerin was similar in NR and SHR. It is concluded that NIF, although acting preferentially in HP as a hypotensive drug, also exerts a slight but still significant effect in NP. The greater vasodilating effect in HP could be due to a supersensitivity of the smooth muscle cell to NIF, possibly located at the calcium influx level.

Animals↗
PubMed1984

A report of seven long survivors for evidence of prognostic factors in hairy cell leukemia.

The clinical hematologic and pathologic findings of 30 patients with hairy cell leukemia observed between 1966 and 1979 were studied. Twelve patients had long-lasting course of the disease. Seven of them displayed a survival greater than or equal to 120 months, whereas 18 patients died within 36 months of the diagnosis. Their clinical and laboratory characteristics (age of onset, sex, ESR, hemoglobin, WBC, neutrophils, monocytes, platelets, spleen and liver size) were analyzed to ascertain possible prognostic features. Multivariate discriminant analysis, performed both with a direct method and with a stepwise method (Wilks' method), provided a discriminant function able to correctly predict the prognosis of the disease in 83.3% of the examined cases. Spleen size, neutrophil count, age of onset, ESR and liver size turned out to be the most important prognostic factors; in contrast, splenectomy did not significantly affect the prognosis in our cases.

Adult↗
PubMed1983

Does acute L-DOPA increase active release of dopamine from dopaminergic neurons?

L-DOPA is believed to be decarboxylated by the residual striatal dopaminergic presynaptic terminals with formation of the putative neurotransmitter dopamine (DA) and with increased availability of DA at post-synaptic receptors. However there is no direct evidence that the DA formed is released into the synaptic cleft. We therefore investigated the biochemical modifications occurring in the dopaminergic system after acute administration of L-DOPA. After acute L-DOPA (100 mg/kg plus 25 mg/kg of benserazide p.o.) the levels of 3-methoxytyramine (3-MT), a metabolite reflecting release of the neurotransmitter DA, were significantly raised, following the same pattern as DA levels, indicating that DA release from DA nerve terminals is increased after L-DOPA administration. The increased DA release and 3-MT formation were not reduced by pretreatment with direct DA agonists such as apomorphine (5 mg/kg i.p.) or piribedil (120 mg/kg p.o.). Thus in this case DA release is not under the control of the compensatory mechanisms induced by post-synaptic receptor hyperstimulation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

The effect of substituted sydnonimines on coronary smooth muscle relaxation and cyclic guanosine monophosphate levels.

In vitro experiments on precontracted canine coronary arteries were performed to study the direct relaxant effects of molsidomine (MOLS) and its active metabolite, SIN-1, and to determine if there is a relationship between effect and cGMP level elevations. The effects of MOLS and SIN-1 were compared with those of a classic vasodilator, nitroglycerin (NTG). At equimolar doses (10(-6)M) SIN-1 exerted greater relaxant effect than NTG (80 +/- 2% and 60 +/- 5%, respectively) in spite of the fact that it produced less of an increase in cyclic guanosine monophosphate (cGMP) levels. cGMP levels fell rapidly after they peaked, but relaxation was maintained. cGMP elevation preceded the induction of relaxation by NTG but not that induced by SIN-1. Relaxation occurred faster after NTG than after SIN-1. Since SIN-1 has a greater relaxant effect than NTG in spite of the fact that SIN-1 induces less of an increase in cGMP levels and the fact that the peak elevation does not precede the onset of relaxation, the causal nexus between GMP level elevation and relaxation effect after sydnonimines should be challenged.

Animals↗
PubMed1982

Effects of angiographic contrast medium on isolated canine coronary arteries.

In isolated canine coronary arteries previously contracted by high potassium concentration, angiographic contrast medium decreased active tension by 61 +/- 2%. The relaxant effect was dose dependent and was not prevented by beta-blockade with d-l-propranolol (10(-5) M). This effect was similar to that obtained with nitroglycerin (10(-6) M), and further relaxation was evident when this vasodilator was administered after exposure to the contrast medium. When arteries were precontracted by alpha-receptor stimulation with norepinephrine (10(-5) M) at normal potassium concentration, a maximal relaxation of 83 +/- 6% was elicited after exposure to contrast medium. The relaxant effect could not be reproduced by a similar increase in osmolarity brought about by addition of sucrose. When arterial strips were processed by radioimmunoassay for dosage of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) after the relaxing action of the contrast medium occurred, a decrease in cAMP from 2.61 +/- 0.86 to 0.63 +/- 0.1 pmol/mg protein (p less than 0.05) was observed, whereas no significant changes in cGMP were detected. These nucleotides do not appear to be involved in the relaxant effect of the dye in the same way as they are when relaxation is elicited by some other coronary vasodilators.

Animals↗