Functional diversity and metabolic response in benthic communities along an ocean acidification gradient.

Altered ocean chemistry caused by ocean acidification (OA) is expected to have negative repercussions at different levels of the ecological hierarchy, starting from the individual and scaling up to the community and ultimately to the ecosystem level. Understanding the effects of OA on benthic organisms is of primary importance given their relevant ecological role in maintaining marine ecosystem functioning. The use of functional traits represents an effective technique to investigate how species adapt to altered environmental conditions and can be used to predict changes in the resilience of communities faced with stresses associated with climate change. Artificial supports were deployed for 1-y along a natural pH gradient in the shallow hydrothermal systems of the Bottaro crater near Panarea (Aeolian Archipelago, southern Tyrrhenian Sea), to explore changes in functional traits and metabolic rates of benthic communities and the repercussions in terms of functional diversity. Changes in community composition due to OA were accompanied by modifications in functional diversity. Altered conditions led to higher oxygen consumption in the acidified site and the selection of species with the functional traits needed to withstand OA. Calcification rate and reproduction were found to be the traits most affected by pH variations. A reduction in a community's functional evenness could potentially reduce its resilience to further environmental or anthropogenic stressors. These findings highlight the ability of the ecosystem to respond to climate change and provide insights into the modifications that can be expected given the predicted future pCO2 scenarios. Understanding the impact of climate change on functional diversity and thus on community functioning and stability is crucial if we are to predict changes in ecosystem vulnerability, especially in a context where OA occurs in combination with other environmental changes and anthropogenic stressors.

Inhibition of sympathetic nerve activity by acute administration of the tricyclic antidepressant desipramine.

In rats anesthetized with pentobarbital/chloral hydrate, the i.v. injection of desipramine (0.3 mg/kg) caused a rapid fall in mean arterial blood pressure accompanied by a reduction in efferent renal nerve integrated activity. A similar reduction in electrical activity was seen in the preganglionic splanchnic nerve. Pretreatment of the rats with yohimbine (0.3 mg/kg) increased renal nerve activity by 20%, and the decrease in blood pressure and renal nerve activity elicited by a subsequent dose of desipramine was blocked. I.v. injection of prazosin (0.05 mg/kg) caused a reduction in systemic blood pressure. The hypotensive effect of a subsequent dose of desipramine was largely blocked, whereas the fall in renal nerve activity was attenuated, but still present. The data are consistent with an action of desipramine to reduce central sympathetic tone by increasing the release of endogenous noradrenaline which acts on alpha 2-adrenoceptors at CNS sites controlling sympathetic activity. An additional involvement of central alpha 1-adrenoceptors cannot be ruled out.

Opposite effects of propafenone and flecainide in a patient with reciprocating supraventricular tachycardia.

A 46 year-old woman with Wolff-Parkinson-White syndrome (postero-septal accessory pathway), symptomatic for recurrent episodes of nonsustained paroxismal supraventricular tachycardia (PSVT), was empirically treated with propafenone (600 mg/day). After a week of therapy the patient returned to the hospital after an episode of syncope. She referred a significant increase in duration and frequency of "palpitations". Under treatment with propafenone a sustained PSVT could be induced during transesophageal testing. During the electrophysiologic study performed off drugs, only a nonsustained PSVT could be induced. After flecainide infusion (1 mg/kg) anterograde block of the accessory pathway was observed and only few beats (less than 8) of PSVT could be induced. The patient was discharged on flecainide (200 mg/day) and 1 month later a transesophageal testing was repeated showing an anterograde block of the accessory pathway at a pacing cycle length of 500 ms; no arrhythmias were induced. The patient has been asymptomatic on chronic oral therapy with flecainide during a follow-up period of 8 months. This case shows that 2 1c class antiarrhythmic drugs may have opposite effects (proarrhythmic and antiarrhythmic). Failure, or even the proarrhythmic effect of one drug, does not necessarily exclude the efficacy of another drug of the same subclass in preventing recurrence of PSVT.

Renal and cardiovascular effects of acute and chronic administration of felodipine to SHR.

Renal function and salt and water turnover were studied in SHR during acute and chronic administration of felodipine, which is an efficient antihypertensive vasodilating Ca2+ antagonist. In conscious SHR acute administration of felodipine in hypotensive doses increased renal sympathetic nerve activity but caused renal vasodilation, increases in GFR and a 2-3 fold increase in urinary flow rate and sodium excretion. The fraction of filtered sodium excreted (FENa) was approximately doubled. The diuretic and natriuretic effects of felodipine are therefore suggested to be due to a direct inhibitory action on the renal tubular cells, resulting in reduced sodium reabsorption. Nifedipine also induced diuresis and natriuresis in this system, while minoxidil reduced water and sodium excretion. Throughout 6 months of felodipine treatment, the mean arterial pressure (MAP), remained 25-20 per cent reduced. Felodipine in combination with metoprolol reduced MAP 25-30 per cent and also caused regression of left ventricular hypertrophy, while felodipine alone prevented its further progression. Also during chronic administration, felodipine induced diuresis but had no effect on plasma volume and on sodium or potassium excretion in SHR. It is concluded that in SHR felodipine induces diuresis; on acute treatment this is secondary to reduced tubular sodium reabsorption, although during chronic treatment the sodium loss is compensated for while the diuresis remains. Thus, the cardiovascular and renal effects of Ca2+ antagonists like felodipine differ substantially from those of other potent antihypertensive vasodilators e.g. minoxidil.

Measurements of plasma norepinephrine concentrations in human primary hypertension. A word of caution on their applicability for assessing neurogenic contributions.

The relationship between plasma levels of norepinephrine (NE) and sympathetic neural activity is discussed with special reference to human primary hypertension. Since sympathetic discharge is differentiated, neural activity to a given target organ will contribute variably to plasma NE levels in different situations. Hemodynamically, early primary hypertension is often characterized by a mild defense reaction-like pattern with signs of increased sympathetic activity to the heart and vasoconstriction in the renal and splanchnic vascular beds. Although important hemodynamically, these organs seem to be of less importance as contributors to peripheral plasma NE levels. In contrast, muscle sympathetic activity and muscle vascular resistance is unchanged or reduced. Since this organ mass contributes importantly to plasma NE levels, especially in peripheral venous blood, it is not surprising that most patients with primary hypertension have normal NE levels. It is concluded that NE concentrations in forearm or mixed venous blood are unreliable indicators of sympathetic neural contributions to essential hypertension, tending to underestimate this element, and that regional measurements of NE overflow are needed for a reliable analysis.

Renal nerve activity and exaggerated natriuresis in conscious spontaneously hypertensive rats.

Exaggerated natriuresis upon volume loading occurs in both human and animal hypertension and is mainly due to suppressed tubular reabsorption. To explore whether altered renal sympathetic activity contributes to this response, conscious male spontaneously hypertensive rats (SHR) were exposed to isotonic saline loading in comparison with normotensive male Wistar Kyoto rats (WKR). After a 60 min control hydropenic period, during which mean arterial pressure, heart rate, renal sympathetic nerve activity and urinary sodium excretion were followed, a 60 min period of intravenous volume expansion with isotonic saline (0.2 ml/min X 100 g b.w.) was started followed by a 60 min hydropenic recovery period. Already during the control period sodium excretion was significantly higher in SHR. During the volume load and subsequent recovery period a clearly exaggerated natriuresis occurred in SHR compared with WKR. Further, volume loading reduced renal sympathetic nerve activity in all animals, but significantly more in SHR. Moreover, volume loading reduced mean arterial pressure and heart rate in both groups. It is suggested that the accentuated reflex inhibition of renal sympathetic activity in SHR upon volume loading emanates from cardiac mechanoreceptors and partly explains the exaggerated natriuresis in SHR. This augmented "volume' reflex response is probably due to reduced systemic venous compliance in SHR with a consequently increased central filling and cardiac receptor activation.

A device for the cutaneous exteriorization of chronic intravascular catheters.

A device has been designed which permits the cutaneous exteriorization of chronically implanted intravascular catheters. From one to three catheters may be exteriorized for withdrawing blood samples or for connecting to a pressure transducer. The device is uniquely suited for studying animals in a conscious and unrestrained state such as during exercise.