In patients hospitalized with decompensated congestive heart failure, nesiritide improves hemodynamic function and clinical status. Nesiritide is useful for the treatment of decompensated congestive heart failure.

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The disulfated peptide growth factor phytosulfokine-α (PSK-α) is perceived by LRR receptor kinases. In this study, a role for PSK signaling through PSK receptor PSKR1 in Arabidopsis thaliana hypocotyl cell elongation is established. Hypocotyls of etiolated pskr1-2 and pskr1-3 seedlings, but not of pskr2-1 seedlings were shorter than wt due to reduced cell elongation. Treatment with PSK-α did not promote hypocotyl growth indicating that PSK levels were saturating. Tyrosylprotein sulfotransferase (TPST) is responsible for sulfation and hence activation of the PSK precursor. The tpst-1 mutant displayed shorter hypocotyls with shorter cells than wt. Treatment of tpst-1 seedlings with PSK-α partially restored elongation growth in a dose-dependent manner. Hypocotyl elongation was significantly enhanced in tpst-1 seedlings at nanomolar PSK-α concentrations. Cell expansion was studied in hypocotyl protoplasts. WT and pskr2-1 protoplasts expanded in the presence of PSK-α in a dose-dependent manner. By contrast, pskr1-2 and pskr1-3 protoplasts were unresponsive to PSK-α. Protoplast swelling in response to PSK-α was unaffected by ortho-vanadate, which inhibits the plasma membrane H+-ATPase. In maize (Zea mays L.), coleoptile protoplast expansion was similarly induced by PSK-α in a dose-dependent manner and was dependent on the presence of K+ in the media. In conclusion, PSK-α signaling of hypocotyl elongation and protoplast expansion occurs through PSKR1 and likely involves K+ uptake, but does not require extracellular acidification by the plasma membrane H+-ATPase.

SUMMARY Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 ± 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a, a') derived from P-V and normalized P-V relations, respectively, for enddiastolic myocardial elastic stiffness (Es or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (Ks or KE) of the circumferential stress-strain relation.Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 ± 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV, dP/dV/V, E. and EE and a tendency for increase in the chamber stiffness constants (a, a') and myocardial stiffness constants (Ks, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid-and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.INCREASED LEFT VENTRICULAR diastolic stiffness has been cited as a cause of elevated left ventricular diastolic pressure, pulmonary venous hypertension and associated symptoms of dyspnea, reduced exercise tolerance and syncope in patients with valvular aortic stenosis.1,2,3 However, quantitation of diastolic stiffness in this common clinical disorder, using both pressure-volume analysis of the ventricular chamber and stress-strain analysis of the myocardial wall, has not been accomplished, pri