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When periodontal disease started to be considered a bacterial infection mainly mediated by subgingival plaque, the basic problem faced by periodontists was the identification and/or quantification of periodontopathogenic bacteria. However, clinical methods continue to be of great value for the diagnosis of periodontal disease. In the present study we show a significant correlation between an index widely used in clinical practice, the Gingival Index of Löe (1967), based on the presence or absence of bleeding on probing, and the methodology of the BANA test for the detection of the specific enzymatic activity of microorganisms involved in periodontal disease. More sensitive and specific clinical parameters, taken together with other microbiologic methods, will be useful in daily clinical practice even before periodontal treatment.

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In the present investigation the ability of subgingival plaque to hydrolyze BANA (Perioscan) was correlated with CPITN scores. Among 281 sites investigated, 136 had a CPITN equal to 2 with a highly significant positive BANA value (107 sites). A CPITN equal to 3 was also significantly BANA positive (90 sites). These findings clearly demonstrate the relationship between CPITN and anaerobic microorganisms (BANA positive).

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Injection of Met-enkephalin (0.05, 0.25 and 0.50 µg in 1 µl) solutions into the lateral hypothalamic area (LHA), of unrestrained and unanesthetized rats caused a significant decrease of sodium (0.30 ñ 0.13 to 0.07 ñ 0.01, P < 0.05) and potassium (0.61 ñ 0.17 to 0.21 ñ 0.04, P < 0.05) excretion. When the blocking agent nalaxone (0.20 µg in 1 µl) was injected alone, a signifricant increase of sodium (0.34 ñ 0.04 to 0.96 ñ 0.28, P < 0.05) and potassium (0.76 ñ 0.13 to 1.72 ñ 0.30, P < 0.05) excretion was observed. However, a dose-response relationship was not observed. However, when in another experiment naloxone was injected before Met-enkepalin into the same area, reversal of the effect of naloxone occured, with decreased sodium and potassium excretion. We conclude that the enkephalinergic pathway of the LHA when stimulated with Met-enkephalin plays an inhibitory role in the contorl of sodium and potassium excretion

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In this study, the participation of the adenylcyclase--cAMP system of the rat septal area in the mediation of the natriuretic, kaliuretic and diuretic effects of noradrenaline (NA) was investigated. The intraseptal injection of 20 nmol of NA caused a significant increase in the urinary excretion of Na+ and K+ as well as in the urinary volume during the 2 hr period following the intracerebral injection which was blocked by 40 nmol of phentolamine, locally injected, 30 min before the catecholamine. In contrast, pretreatment with propranolol (100 nmol) potentiated the effects of NA on salt and water renal excretion. The intraseptal injection of 3.12 to 50 nmol of dibutryrl cyclic adenosine monophosphate (db cAMP) caused dose-dependent increase in natriuresis and kaliuresis, but a decrease in urinary volume. Under the same experimental conditions, caffeine administration (6.25 to 100 nmol) also induced dose-dependent increases in Na+ and K+ urinary output. These results indicate that the saluretic effect of NA may be mediated by an alpha receptor-induced activation of the adenylcyclase--cAMP system in the septal area.

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The effect of intraseptal injection of carbachol and nicotine on urinary output of Na+ and K+ in untreated rats as well as in animals pretreated with locally injected atropine, hexamethonium, dibenamine and propranolol was studied in order to evaluate the relative role played by central muscarinic and nicotinic receptors in the regulation of salt and water renal excretion. The injection of 30-250 nmol of nicotine into the medial septal area caused a dose-dependent increase in Na+ and K+ urinary output whereas urine volume was little affected. The effect of 30 nmol of nicotine was blocked by pretreatment with 100 nmol of hexamethonium. In addition, pretreatment with 5 nmol of either hexamethonium or atropine partially antagonized the natriuretic and kaliuretic effect of 1 nmol of carbachol. Also the alpha-blocking agent, dibenamine (150 nmol) antagonized, while the beta-blocker, propranolol (100 nmol) significantly enhanced the effect of carbachol. Propranolol (100 nmol) alone caused a small, but significant increase in Na+ and K+ renal excretion. These results indicate that stimulation of both muscarinic and nicotinic receptors in the septal area, as caused by carbachol, elicits increased disposition of Na+ and K+ by the kidneys. Also, part of the effects of carbachol appear to be mediated by the release of endogenous catecholamines, acting on central alpha receptors to increase Na+ and K+ urinary excretion. On the other hand, simultaneous activation of beta-receptors by the released amines would partially inhibit this effect.

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