Electronic structure of nitric oxide adducts of bis(diaryl-1,2-dithiolene)iron compounds: four-membered electron-transfer series [Fe(NO)(L)2]z (z = 1+, 0, 1-, 2-).

Four members of the electron-transfer series [Fe(NO)(S(2)C(2)R(2))2]z (z = 1+, 0, 1-, 2-) have been isolated as solid materials (R = p-tolyl): [1a](BF4), [1a]0, [Co(Cp)2][1a], and [Co(Cp)2]2[1a]. In addition, complexes [2a]0 (R = 4,4-diphenyl), [3a]0 (R = p-methoxyphenyl), [Et(4)N][4a] (R = phenyl), and [PPh(4)][5a] (R = -CN) have been synthesized and the members of each of their electron-transfer series electrochemically generated in CH(2)Cl(2) solution. All species have been characterized electro- and magnetochemically.

Electronic structure of mononuclear bis(1,2-diaryl-1,2-ethylenedithiolato)iron complexes containing a fifth cyanide or phosphite ligand: a combined experimental and computational study.

A series of mononuclear square-based pyramidal complexes of iron containing two 1,2-diaryl-ethylene-1,2-dithiolate ligands in various oxidation levels has been synthesized. The reaction of the dinuclear species [Fe(III)2(1L*)2(1L)2]0, where (1L)2- is the closed shell di-(4-tert-butylphenyl)-1,2-ethylenedithiolate dianion and (1L*)1- is its one-electron-oxidized pi-radical monoanion, with [N(n-Bu)4]CN in toluene yields dark green crystals of mononuclear [N(n-Bu)4][Fe(II)(1L*)2(CN)] (1). The oxidation of 1 with ferrocenium hexafluorophosphate yields blue [Fe(III)(1L*)2(CN)] (1ox), and analogously, a reduction with [Cp2Co] yields [Cp2Co][N(n-Bu)4][Fe(II)(1L*)(1L)(CN)] (1red); oxidation of the neutral dimer with iodine gives [Fe(III)(1L*)2I] (2).

Dinuclear Bis(1,2-diaryl-1,2-ethylenedithiolato)iron complexes: [FeIII2(L)4]n (n = 2-, 1-, 0, 1+).

The electronic structures of four members of the electron-transfer series [Fe2(1L)4]n (n = 2-, 1-, 0, 1+) have been elucidated in some detail by electronic absorption, IR, X-band electron paramagnetic resonance (EPR), and Mössbauer spectroscopies where (1L)(2-) represents the ligand 1,2-bis(4-tert-butylphenyl)-1,2-ethylenedithiolate(2-) and (1L*)- is its pi-radical monoanion. It is conclusively shown that all redox processes are ligand-centered and that high-valent iron(IV) is not accessible. The following complexes have been synthesized: [FeIII2(1L*)2(1L)2]0 (1), [FeIII2(2L*)2(2L)2].

Role of VIP in the regulation of LH secretion in the female rat.

Vasoactive intestinal peptide (VIP) is found within neurons throughout the body. It influences the secretion of several hormones of the anterior pituitary by neural and pituitary actions. We review work from our laboratory that indicates that VIP inhibits the secretion of luteinizing hormone (LH) by a hypothalamic action.

Effect of [4Cl-D-Phe6,Leu17]VIP on the inhibition of pulsatile LH release by VIP and related peptides in the ovariectomized rat.

Pulsatile LH secretion in the ovariectomized (OVX) rat is inhibited by intracerebroventricular (icv) infusion of vasoactive intestinal peptide (VIP). VIP, rat growth hormone-releasing hormone (rGRH) and secretin with and without an antagonist to VIP, [4Cl-D-Phe6,Leu17]VIP (VIPA), were infused icv into OVX rats. Both VIP and rGRH at an infusion rate of 3.

Vasoactive intestinal peptide inhibits the steroid-induced LH surge in the ovariectomized rat.

The LH surge was induced in ovariectomized rats by sequential treatment with oestradiol benzoate and progesterone. Vasoactive intestinal peptide (VIP) or saline was infused into the third cerebral ventricle from 13.30 to 16.

Differential glucocorticoid regulation of glucagon gene expression in cell lines derived from rat and hamster islet cell tumors.

Glucocorticoid regulation of peptide hormone gene expression was studied in two cell lines derived from rodent islet cell tumors. In rat RIN1056A cells, dexamethasone reduced the levels of glucagon mRNA transcripts while markedly inducing the expression of the angiotensinogen gene. In contrast, dexamethasone had no effect on the regulation of glucagon gene expression in hamster InR1-G9 cells.

The rat glucagon gene is regulated by a protein kinase A-dependent pathway in pancreatic islet cells.

A cAMP response element (CRE) has been identified in the proximal 5'-flanking region of the rat glucagon gene, and activation of the cAMP-dependent pathway in fetal rat intestinal cells leads to an increase in the levels of glucagon mRNA transcripts. In contrast, the human glucagon gene does not contain a similar CRE, and the results of studies using immortalized rat and hamster islet cell lines have suggested that glucagon gene expression may not be regulated by cAMP. To reconcile these observations, we have studied the control of glucagon gene expression.

Proglucagon-derived peptides in the neuroendocrine system.

Using several novel in vitro culture systems, we have examined the tissue-specific regulation of the proglucagon-derived peptides, at the levels of proglucagon gene expression and pGdp synthesis and secretion. Our studies indicate that proglucagon gene expression in intenstine, hypothalamus and pancreas is under the regulatory control of protein kinase A- but not a protein kinase C-dependent pathway. PKA and PKC stimulate secretion of the intestinal pGdp's, whereas only PKA stimulates secretion of the hypothalamic peptides.

Effects of lesions of the suprachiasmatic and paraventricular nuclei on the inhibition of pulsatile luteinizing hormone release by exogenous vasoactive intestinal peptide in the ovariectomized rat.

Vasoactive intestinal peptide (VIP) inhibits pulsatile luteinizing hormone (LH) secretion in the ovariectomized rat. Hypothalamic nuclei known to contain VIPergic neurons were destroyed electrolytically to determine whether either an increased response or a loss of response to exogenous VIP would result. Bilateral electrolytic lesions were made of either the suprachiasmatic (SCN) or paraventricular (PVN) nuclei in separate experiments; all animals received an intracerebroventricular cannula at the same time.

Vasoactive intestinal peptide inhibits luteinizing hormone secretion: the inhibition is not mediated by dopamine.

Vasoactive intestinal peptide (VIP) is a neuropeptide that is present in the hypothalamus and is probably a neuroendocrine regulator. The effect of VIP on pulsatile LH secretion in the long-term ovariectomized rat was re-examined in the light of earlier conflicting reports. VIP or saline was infused into the third ventricle at the rat of 15 microliters/h and blood was sampled frequently before and during the infusion.

Serotonin stimulates prolactin secretion in the hypophysectomized adenohypophyseal grafted rat.

Normal male, oestrogen (F2) primed male and hypophysectomized adenohypophyseal grafted male rats (HAG rats) were used in the experiments. Serotonin creatinine sulphate was injected as a bolus via an indwelling atrial cannula in the conscious free moving rat. Serotonin caused a dose-dependent increase in plasma prolactin (Prl) in normal (1, 3 and 10 mg/kg serotonin) and E2 primed (1 and 3 mg/kg serotonin) male rats that began immediately after injection and reached a peak within 12-15 min of injection.